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Research ArticleExperimental Studies
Open Access

DDX39 Is Down-regulated in Chromophobe Renal Cell Carcinoma Tissues, Whereas Overexpression Is Associated With Shorter Patient Survival

SHIN-NOSUKE YAMASHITA, YOSHIATSU TANAKA, SHAJEDUL ISLAM, TAKAO KITAGAWA, KAZUHIRO TOKUDA, DURGA PAUDEL, SARITA GIRI, TOHRU OHTA, FUMIYA HARADA, HIROKI NAGAYASU and YASUHIRO KURAMITSU
Anticancer Research November 2025, 45 (11) 4743-4749; DOI: https://doi.org/10.21873/anticanres.17823
SHIN-NOSUKE YAMASHITA
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
2Division of Oral and Maxillofacial Surgery School of Dentistry, Ishikari-Tobetsu, Japan;
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YOSHIATSU TANAKA
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
2Division of Oral and Maxillofacial Surgery School of Dentistry, Ishikari-Tobetsu, Japan;
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SHAJEDUL ISLAM
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
3Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.;
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TAKAO KITAGAWA
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
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KAZUHIRO TOKUDA
4Graduate School of Health and Welfare, Yamaguchi Prefectural University, Yamaguchi, Japan
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DURGA PAUDEL
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
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SARITA GIRI
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
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TOHRU OHTA
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
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FUMIYA HARADA
2Division of Oral and Maxillofacial Surgery School of Dentistry, Ishikari-Tobetsu, Japan;
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HIROKI NAGAYASU
2Division of Oral and Maxillofacial Surgery School of Dentistry, Ishikari-Tobetsu, Japan;
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YASUHIRO KURAMITSU
1Advanced Research Promotion Centre, Ishikari-Tobetsu, Japan;
5School of Medical Technology, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Japan;
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  • For correspondence: climates{at}hoku-iryo-u.ac.jp
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Abstract

Background/Aim: Renal cell carcinoma (RCC) accounts for 85% of kidney tumors, and its incidence is rising. It includes 14 histological subtypes, notably clear cell (KIRC), papillary (KIRP), and chromophobe (KICH) RCC. While RCC generally has a favorable prognosis, the 5-year survival rate drops to ~12% with distant metastasis. Identifying prognostic markers is therefore crucial. DDX39, a DEAD-box RNA helicase, is up-regulated in various cancers, but its prognostic role in KIRP and KICH remains unclear. This study investigates the clinical relevance of DDX39 expression in KIRC, KIRP, and KICH using TCGA bioinformatics data.

Materials and Methods: The University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) platform was used to analyze DDX39 mRNA expression and survival in patients with KIRC, KIRP and KICH from The Cancer Genome Atlas (TCGA) database.

Results: DDX39 mRNA levels were found to be significantly higher in KIRC and KIRP tissues compared to normal kidney tissues, and this up-regulation was inversely correlated with prolonged survival in KIRC and KIRP patients. However, DDX39 mRNA levels in KICH tissues were significantly lower than those in normal kidney tissues. Nevertheless, patients with high DDX39 mRNA expression in KICH tissues had significantly shorter survival times.

Conclusion: Although the expression levels of DDX39 mRNA in tumor tissues varies depending on the tissue type, expression is inversely correlated with patient prognosis, making it a promising prognostic factor in RCC, including KICH.

Keywords:
  • DDX39
  • chromophobe renal cell carcinoma
  • clear cell renal cell carcinoma
  • papillary renal cell carcinoma
  • TCGA

Introduction

Renal cell carcinoma (RCC) arises from tubular epithelial cells. Worldwide, RCC is the sixth most commonly diagnosed cancer in men and the tenth most commonly diagnosed cancer in women, accounting for approximately 2% of cancer diagnoses and deaths. More than 140,000 patients die from RCC each year (1, 2). If RCC is detected early, the prognosis is good with a 5-year survival rate of 93%, but once metastasis is detected, the 5-year survival rate plummets to 12% (3). Therefore, identifying prognostic factors for RCC may be of great importance in predicting patient outcomes. RCC is divided into several types based on histological type; the most common is clear cell renal cell carcinoma (KIRC), which accounts for approximately 70-80% of cases, followed by papillary renal cell carcinoma (KIRP), which accounts for approximately 10-15%, and chromophobe renal cell carcinoma (KICH), which accounts for approximately 5%. KIRC and KIRP are thought to arise primarily from the proximal tubules, whereas KICH is thought to arise primarily from the distal connecting tubules and collecting duct system (4). KIRC has the poorest prognosis and is characterized by metastases to the lungs, liver and bones (5). KIRP has a better prognosis compared to KIRC, and KICH has the best prognosis, as metastases occur in only 7% of cases (1).

DDX39 is an Asp-Glu-Ala-Asp (DEAD) box RNA helicase that is essential for unwinding double-stranded RNA molecules, transcription, splicing, RNA transport, ribosome biogenesis, RNA editing, RNA degradation, translation, and telomere protection and maintenance (6-8).

Overexpression of DDX39 in tumor tissues and cells has been reported in multiple cases including human lung squamous cell carcinoma tissues (9), gastrointestinal stromal tumor tissues from patients with poor prognosis (10), urinary bladder cancer tissues (11) human malignant pleural mesothelioma cells (12), clear cell renal cell carcinoma tissues (13), and human gemcitabine-resistant pancreatic cancer cells (14), and we have reported that high expression of DDX39 is associated with a significantly poor prognosis in adrenocortical carcinoma and uveal melanoma. However, the role of DDX39 in cancer cells remains unclear (15, 16). As mentioned above, Kato et al. demonstrated that DDX39 has the effect of suppressing the invasion of bladder cancer cells (11). On the other hand, there are many papers stating that DDX39 may have a negative impact on patient prognosis (9, 10, 12-14, 17). The impact of DDX39 on patient prognosis may vary depending on the type of cancer. However, the association between DDX39 expression and prognosis in patients with KIRP and KICH has not yet been reported. This study aimed to clarify the clinical significance of DDX39 expression in patients with three types of renal cell carcinoma: KIRC, KIRP, and KICH, using bioinformatics of the TCGA dataset.

Materials and Methods

mRNA expression of DDX39 in clear cell renal cell carcinoma, papillary renal cell carcinoma, and chromophobe renal cell carcinoma tissues. To investigate DDX39 mRNA expression levels in clear cell renal cell carcinoma (KIRC), papillary renal cell carcinoma (KIRP), and chromophobe renal cell carcinoma (KICH) tissues. The University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) (18), a web server for cancer and normal gene expression profiling, was used. DDX39 mRNA expression levels in cancer tissues of KIRC, KIRP, and KICH patients were investigated from The Cancer Genome Atlas (TCGA) database using the UALCAN platform. In the TCGA database, the gene name “DDX39” was entered. A p-value <0.05 was considered statistically significant (Figure 1).

Figure 1.
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Figure 1.

Flow chart for bioinformatics analyses from (The Cancer Genome Atlas) TCGA database using the UALCAN platform.

Survival analysis according to mRNA expression levels of DDX39 in clear cell renal cell carcinoma, papillary renal cell carcinoma, and chromophobe renal cell carcinoma tissues. Survival analysis was performed to examine DDX39 expression in KIRC, KIRP, and KICH tissues using the UALCAN platform. The gene name “DDX39” was entered into the TCGA database, and a median cutoff was selected to generate Kaplan-Meier curves for KIRC, KIRP, and KICH patients. A p-value <0.05 was considered statistically significant (Figure 1).

Results

DDX39 mRNA expression was increased in clear cell renal cell carcinoma and papillary renal cell carcinoma tissues. To assess whether DDX39 mRNA expression is increased in KIRC tissues, we analyzed the TCGA dataset using the UALCAN platform. The results showed that the expression of DDX39 mRNA was increased in KIRC tissues (n=533) compared to normal tissues (n=72) (p=1.62447832963153E-12) (Figure 2A). We then analyzed the mRNA expression of DDX39 in KIRP tissues using UALCAN, which showed that, similar to KIRC tissues, the mRNA expression of DDX39 in KIRP tissues (n=290) was significantly higher than that in normal kidney tissues (n=32) (p=1.67665881178891E-12) (Figure 3A).

Figure 2.
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Figure 2.

DDX39 mRNA expression analysis for clear cell renal cell carcinoma tissues from The Cancer Genome Atlas (TCGA) database using University of Alabama at Birmingham CANcer data analysis (UALCAN) platform. (A) Boxplots were obtained from the UALCAN portal, utilizing data from the TCGA for clear cell renal cell carcinoma (KIRC). The left box represents normal kidney tissues (n=72), while the right box corresponds to KIRC tissues (n=533). The observed difference was statistically significant (p=1.62×10−12), with p<0.05 considered significant. (B) Overall survival analysis based on DDX39 expression level was performed using the UALCAN platform. Overall survival curves of KIRC patients were compared between the DDX39 high expression group (▲, n=133) and the low/medium expression group (n=398) (p=0.00014). p<0.05 was considered statistically significant.

Figure 3.
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Figure 3.

DDX39 mRNA expression analysis for papillary renal cell carcinoma tissues from The Cancer Genome Atlas (TCGA) database using University of Alabama at Birmingham CANcer data analysis (UALCAN) platform. (A) Boxplots were obtained from the UALCAN portal, utilizing data from the TCGA for papillary renal cell carcinoma (KIRP). The left box represents normal kidney tissues (n=39), wherein the right box represents KIRP tissues (n=290) (p=1.67×10−12). p<0.05 was regarded as statistically significant. (B) Overall survival analysis based on DDX39 expression level was performed using the UALCAN platform. Overall survival curves of KIRP patients were compared between the DDX39 high expression group (▲, n=73) and the low/medium expression group (n=214) (p=0.00025). p<0.05 was considered statistically significant.

High levels of DDX39 expression in clear cell renal cell carcinoma and papillary renal cell carcinoma tissues are inversely correlated with prolonged patient survival. Kaplan-Meier survival plots of patients with high and low DDX39 expression levels in KIRC and KIRP tissues were generated using UALCAN platform. The results showed that increasing DDX39 expression levels in cancer tissues were inversely correlated with prolonged patient survival with KIRC (p=0.00014) (Figure 2B) and KIRP (p=0.00025) (Figure 3B).

DDX39 mRNA expression was decreased in chromophobe renal cell carcinoma tissues. The results of DDX39 mRNA expression analysis of TCGA dataset using UALCAN platform revealed that, unlike KIRK and KIRP, DDX39 mRNA expression was significantly decreased in KICH tissues (n=67) compared to normal kidney tissues (n=25) (p=5.188100E-04) (Figure 4A).

Figure 4.
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Figure 4.

DDX39 mRNA expression analysis for chromophobe renal cell carcinoma tissues from The Cancer Genome Atlas (TCGA) database using University of Alabama at Birmingham CANcer data analysis (UALCAN) platform. (A) Boxplots were obtained from the UALCAN portal, utilizing data from the TCGA for chromophobe renal cell carcinoma (KICH). The left box represents normal kidney tissues (n=25), wherein the right box represents KICH tissues (n=67) (p=5.188100E-04). p<0.05 was regarded as statistically significant. (B) Overall survival analysis based on DDX39 expression level was performed using the UALCAN platform. Overall survival curves of KICH patients were compared between the DDX39 high expression group (▲, n=17) and the low/medium expression group (n=48) (p=0.0015). p<0.05 was considered statistically significant.

High expression of DDX39 expression in chromophobe renal cell carcinoma tissues is inversely correlated with prolonged patient survival. Kaplan-Meier survival plots of patients with high and low DDX39 expression levels in KICH tissues were generated using UALCAN platform. The results showed that increased expression levels of DDX39 in KICH tissues were inversely correlated with prolonged survival of KICH patients (p=0.0015) (Figure 4B).

Discussion

In this study, we used the UALCAN bioinformatics platform to analyze DDX39 mRNA expression and Kaplan-Meier survival rates in patients with KIRC, KIRP, and KICH. DDX39 mRNA expression levels were significantly higher in KIRC and KIRP tissues than in normal tissues, but lower in KICH tissues compared to normal kidney tissues. Furthermore, KIRC, KIRP, and KICH patients with high DDX39 mRNA expression were shown to have poor prognosis.

Although it is not possible to simply determine the relationship between the expression level of DDX39 in cancer tissues and prognosis, a significant correlation was observed between the prognosis of patients with the three types of RCC examined in this study, KIRC, KIRP, and KICH, and the expression level of DDX39 mRNA. Bao et al. reported that DDX39 expression was elevated in both the public database and the database of KIRC patients at Changhai Hospital, and high DDX39 expression was inversely correlated with the prognosis of KIRC patients. Although the relationship between DDX39 and the prognosis of KIRP and KICH patients has not been investigated by them, DDX39 definitely influences poor prognosis in KIRC patients (13). In a study of 72 patients with gastrointestinal stromal tumors (GIST), Kikuta et al. identified DDX39 as a biomarker for GIST that may be associated with metastatic disease and poor clinical outcome (10). On the other hand, Ma et al. reported that patients with low expression of DDX39 in colorectal cancer tissues had a poor prognosis (19). Furthermore, Kato et al. found that DDX39 was overexpressed in bladder cancer tissues compared to control normal tissues by comparative proteomic analysis of bladder cancer and normal mucosa. Immunohistochemical analysis of 303 bladder cancer specimens showed that the expression level of DDX39 was inversely correlated with pT stage and histological progression. Furthermore, bladder cancer cells with DDX39 knockdown had increased invasive potential compared to control cells (11). Therefore, it is thought that the relationship between the expression level of DDX39 and prognosis differs depending on the type of cancer.

Although it is true that high expression of DDX39 in KIRC, KIRP, and KICH tissues is indeed associated with poor patient prognosis, the reason why the expression of DDX39 in KICH is lower than that in normal renal tissues remains unclear.

Molecules that have been reported to be specifically expressed in KICH tumor tissues and cells include BSND, which is involved in the reabsorption of chloride ions, and ATP6V1G3, which controls acid-base balance. BSND showed a 100% positive protein expression rate in KICH, while KIRC and KIRP were both negative, suggesting that it is a molecule specific to KICH (20).

In addition, Wang et al. reported that defensin beta 1, a peptide factor involved in host defense, was highly expressed in KICH (21), and Li et al. showed that Alpha-2-Heremans-Schmid glycoprotein was highly expressed in KICH and may be a potential therapeutic target and prognostic gene marker (22). Cioca et al. reported that Galectin-3 is highly expressed in the nucleus of KICH cells and is an indicator of malignancy (23). Conversely, Molnar et al. reported that FOXI1 is expressed in only 3% of KICH cells but did not mention its association with prognosis (24). However, there are no reports of molecules whose expression in KICH tissue is attenuated compared to the surrounding normal tissue, and whose increased expression leads to a worse prognosis for patients. If there is a possibility, it is possible that DDX39 expression is low because KICH is a cancer with a good prognosis among RCC. However, as the malignancy progresses, DDX39 expression also increases, and ultimately this may be the cause of a worse prognosis. Because metastasis of KICH occurs in only 7% of cases (1), it may be necessary to confirm the expression of DDX39 in primary KICH tissues from metastatic cases. Molnar et al. reported that eosinophilic variant is a highly malignant variant of KICH, so the expression of DDX39 in eosinophilic variant of KICH cells may also be of interest (25). Further studies are needed to clarify the exact mechanisms by which DDX39 promotes the progression of KIRC, KIRP, and KICH.

This present study suggested that high expression of DDX39 may be associated with poor prognosis in KIRC, KIRP, and KICH patients, but no studies have reported whether prognosis can be predicted by detecting DDX39 in human urine. If DDX39 could be quantitatively detected in the urine of KIRC, KIRP, and KICH patients, it may be possible to predict prognosis without invasive clinical testing, which would be extremely convenient for patients.

Footnotes

  • Authors’ Contributions

    All Authors contributed to the conception and design of the study. Data collection and analysis were performed by Shin-nosuke Yamashita, Yoshiatsu Tanaka, Shajedul Islam and Yasuhiro Kuramitsu. Shin-nosuke Yamashita and Yoshiatsu Tanaka wrote the first draft of the manuscript, Takao Kitagawa and Yasuhiro Kuramitsu commented on an earlier version of the manuscript. All Authors read and approved the final manuscript.

  • Conflicts of Interest

    The Authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

  • Artificial Intelligence (AI) Disclosure

    No artificial intelligence (AI) tools, including large language models or machine learning software, were used in the preparation, analysis, or presentation of this manuscript.

  • Received July 1, 2025.
  • Revision received July 15, 2025.
  • Accepted July 25, 2025.
  • Copyright © 2025 The Author(s). Published by the International Institute of Anticancer Research.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

References

  1. ↵
    1. Capitanio U,
    2. Bensalah K,
    3. Bex A,
    4. Boorjian SA,
    5. Bray F,
    6. Coleman J,
    7. Gore JL,
    8. Sun M,
    9. Wood C,
    10. Russo P
    : Epidemiology of renal cell carcinoma. Eur Urol 75(1): 74-84, 2019. DOI: 10.1016/j.eururo.2018.08.036
    OpenUrlCrossRefPubMed
  2. ↵
    1. Padala SA,
    2. Barsouk A,
    3. Thandra KC,
    4. Saginala K,
    5. Mohammed A,
    6. Vakiti A,
    7. Rawla P,
    8. Barsouk A
    : Epidemiology of renal cell carcinoma. World J Oncol 11(3): 79-87, 2020. DOI: 10.14740/wjon1279
    OpenUrlCrossRefPubMed
  3. ↵
    1. Siegel RL,
    2. Miller KD,
    3. Jemal A
    : Cancer statistics, 2017. CA Cancer J Clin 67(1): 7-30, 2017. DOI: 10.3322/caac.21387
    OpenUrlCrossRefPubMed
  4. ↵
    1. Warren AY,
    2. Harrison D
    : WHO/ISUP classification, grading and pathological staging of renal cell carcinoma: standards and controversies. World J Urol 36(12): 1913-1926, 2018. DOI: 10.1007/s00345-018-2447-8
    OpenUrlCrossRefPubMed
  5. ↵
    1. Chevrier S,
    2. Levine JH,
    3. Zanotelli VRT,
    4. Silina K,
    5. Schulz D,
    6. Bacac M,
    7. Ries CH,
    8. Ailles L,
    9. Jewett MAS,
    10. Moch H,
    11. van den Broek M,
    12. Beisel C,
    13. Stadler MB,
    14. Gedye C,
    15. Reis B,
    16. Pe’er D,
    17. Bodenmiller B
    : An immune atlas of clear cell renal cell carcinoma. Cell 169(4): 736-749.e18, 2017. DOI: 10.1016/j.cell.2017.04.016
    OpenUrlCrossRefPubMed
  6. ↵
    1. De La Cruz J,
    2. Kressler D,
    3. Linder P
    : Unwinding RNA in Saccharomyces cerevisiae: DEAD-box proteins and related families. Trends Biochem Sci 24(5): 192-198, 1999. DOI: 10.1016/s0968-0004(99)01376-6
    OpenUrlCrossRefPubMed
    1. Rocak S,
    2. Linder P
    : DEAD-box proteins: the driving forces behind RNA metabolism. Nat Rev Mol Cell Biol 5(3): 232-241, 2004. DOI: 10.1038/nrm1335
    OpenUrlCrossRefPubMed
  7. ↵
    1. Yoo HH,
    2. Chung IK
    : Requirement of DDX39 DEAD box RNA helicase for genome integrity and telomere protection. Aging Cell 10(4): 557-571, 2011. DOI: 10.1111/j.1474-9726.2011.00696.x
    OpenUrlCrossRefPubMed
  8. ↵
    1. Sugiura T,
    2. Nagano Y,
    3. Noguchi Y
    : DDX39, upregulated in lung squamous cell cancer, displays RNA helicase activities and promotes cancer cell growth. Cancer Biol Ther 6(6): 957-964, 2007. DOI: 10.4161/cbt.6.6.4192
    OpenUrlCrossRefPubMed
  9. ↵
    1. Kikuta K,
    2. Kubota D,
    3. Saito T,
    4. Orita H,
    5. Yoshida A,
    6. Tsuda H,
    7. Suehara Y,
    8. Katai H,
    9. Shimada Y,
    10. Toyama Y,
    11. Sato K,
    12. Yao T,
    13. Kaneko K,
    14. Beppu Y,
    15. Murakami Y,
    16. Kawai A,
    17. Kondo T
    : Clinical proteomics identified ATP-dependent RNA helicase DDX39 as a novel biomarker to predict poor prognosis of patients with gastrointestinal stromal tumor. J Proteomics 75(4): 1089-1098, 2012. DOI: 10.1016/j.jprot.2011.10.005
    OpenUrlCrossRefPubMed
  10. ↵
    1. Kato M,
    2. Wei M,
    3. Yamano S,
    4. Kakehashi A,
    5. Tamada S,
    6. Nakatani T,
    7. Wanibuchi H
    : DDX39 acts as a suppressor of invasion for bladder cancer. Cancer Sci 103(7): 1363-1369, 2012. DOI: 10.1111/j.1349-7006.2012.02298.x
    OpenUrlCrossRefPubMed
  11. ↵
    1. Kuramitsu Y,
    2. Tominaga W,
    3. Baron B,
    4. Tokuda K,
    5. Wang Y,
    6. Kitagawa T,
    7. Nakamura K
    : Up-regulation of DDX39 in human malignant pleural mesothelioma cell lines compared to normal pleural mesothelial cells. Anticancer Res 33(6): 2557-2560, 2013.
    OpenUrlAbstract/FREE Full Text
  12. ↵
    1. Bao Y,
    2. Jiang A,
    3. Dong K,
    4. Gan X,
    5. Gong W,
    6. Wu Z,
    7. Liu B,
    8. Bao Y,
    9. Wang J,
    10. Wang L
    : DDX39 as a predictor of clinical prognosis and immune checkpoint therapy efficacy in patients with clear cell renal cell carcinoma. Int J Biol Sci 17(12): 3158-3172, 2021. DOI: 10.7150/ijbs.62553
    OpenUrlCrossRefPubMed
  13. ↵
    1. Kuramitsu Y,
    2. Suenaga S,
    3. Wang Y,
    4. Tokuda K,
    5. Kitagawa T,
    6. Tanaka T,
    7. Akada J,
    8. Maehara S,
    9. Maehara Y,
    10. Nakamura K
    : Up-regulation of DDX39 in human pancreatic cancer cells with acquired gemcitabine-resistance compared to gemcitabine-sensitive parental cells. Anticancer Res 33(8): 3133-3136, 2013.
    OpenUrlAbstract/FREE Full Text
  14. ↵
    1. Tanaka Y,
    2. Yamashita SN,
    3. Islam S,
    4. Kitagawa T,
    5. Tokuda K,
    6. Paudel D,
    7. Giri S,
    8. Ohta T,
    9. Harada F,
    10. Nagayasu H,
    11. Kuramitsu Y
    : Up-regulated DDX39 in adrenocortical carcinoma is associated with patient survival. Anticancer Res 45(2): 811-815, 2025. DOI: 10.21873/anticanres.17469
    OpenUrlAbstract/FREE Full Text
  15. ↵
    1. Yamashita SN,
    2. Tanaka Y,
    3. Islam S,
    4. Kitagawa T,
    5. Tokuda K,
    6. Paudel D,
    7. Giri S,
    8. Ohta T,
    9. Harada F,
    10. Nagayasu H,
    11. Kuramitsu Y
    : Increased expression of DDX39 in uveal melanoma is associated with patient prognosis. Anticancer Res 45(4): 1661-1666, 2025. DOI: 10.21873/anticanres.17547
    OpenUrlAbstract/FREE Full Text
  16. ↵
    1. Wang X,
    2. Li P,
    3. Wang C,
    4. Zhang D,
    5. Zeng L,
    6. Liu X,
    7. Lin J
    : DEAD-box RNA helicase 39 promotes invasiveness and chemoresistance of ER-positive breast cancer. J Cancer 11(7): 1846-1858, 2020. DOI: 10.7150/jca.37247
    OpenUrlCrossRefPubMed
  17. ↵
    1. Chandrashekar DS,
    2. Karthikeyan SK,
    3. Korla PK,
    4. Patel H,
    5. Shovon AR,
    6. Athar M,
    7. Netto GJ,
    8. Qin ZS,
    9. Kumar S,
    10. Manne U,
    11. Creighton CJ,
    12. Varambally S
    : UALCAN: An update to the integrated cancer data analysis platform. Neoplasia 25: 18-27, 2022. DOI: 10.1016/j.neo.2022.01.001
    OpenUrlCrossRefPubMed
  18. ↵
    1. Ma J,
    2. Chang W,
    3. Zhang W
    : [Relationship between the expression of DDX39 protein and prognosis of colorectal cancer]. Zhonghua Wei Chang Wai Ke Za Zhi 21(3): 336-341, 2018.
    OpenUrlPubMed
  19. ↵
    1. Shinmura K,
    2. Igarashi H,
    3. Kato H,
    4. Koda K,
    5. Ogawa H,
    6. Takahashi S,
    7. Otsuki Y,
    8. Yoneda T,
    9. Kawanishi Y,
    10. Funai K,
    11. Takayama T,
    12. Ozono S,
    13. Sugimura H
    : BSND and ATP6V1G3: novel immunohistochemical markers for chromophobe renal cell carcinoma. Medicine (Baltimore) 94(24): e989, 2015. DOI: 10.1097/MD.0000000000000989
    OpenUrlCrossRefPubMed
  20. ↵
    1. Wang L,
    2. Yang H,
    3. Cao L,
    4. Yang Y,
    5. Ding R
    : Integrative genomic pan-cancer analysis reveals the prognostic significance of DEFB1 in tumors. Discov Oncol 16(1): 552, 2025. DOI: 10.1007/s12672-025-02340-6
    OpenUrlCrossRefPubMed
  21. ↵
    1. Li X,
    2. Ma C
    : Alpha-2-Heremans-Schmid-glycoprotein (AHSG) a potential biomarker associated with prognosis of chromophobe renal cell carcinoma: The PROPOLIS study. Health Sci Rep 5(6): e878, 2022. DOI: 10.1002/hsr2.878
    OpenUrlCrossRef
  22. ↵
    1. Cioca A,
    2. Muntean D,
    3. Bungardean C,
    4. Raica M,
    5. Cimpean AM
    : Expression and distribution of Galectin-3 in chromophobe and papillary carcinomas. Anticancer Res 38(1): 259-263, 2018. DOI: 10.21873/anticanres.12216
    OpenUrlAbstract/FREE Full Text
  23. ↵
    1. Molnar A,
    2. Horvath CA,
    3. Czovek P,
    4. Szanto A,
    5. Kovacs G
    : FOXI1 immunohistochemistry differentiates benign renal oncocytoma from malignant chromophobe renal cell carcinoma. Anticancer Res 39(6): 2785-2790, 2019. DOI: 10.21873/anticanres.13405
    OpenUrlAbstract/FREE Full Text
  24. ↵
    1. Molnar A,
    2. Yusenko MV,
    3. Kovacs G,
    4. Banyai D
    : The role of genetic analysis in correct diagnosis of eosinophilic variant of chromophobe renal cell carcinoma. Anticancer Res 40(12): 6863-6867, 2020. DOI: 10.21873/anticanres.14708
    OpenUrlAbstract/FREE Full Text
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Anticancer Research: 45 (11)
Anticancer Research
Vol. 45, Issue 11
November 2025
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DDX39 Is Down-regulated in Chromophobe Renal Cell Carcinoma Tissues, Whereas Overexpression Is Associated With Shorter Patient Survival
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DDX39 Is Down-regulated in Chromophobe Renal Cell Carcinoma Tissues, Whereas Overexpression Is Associated With Shorter Patient Survival
SHIN-NOSUKE YAMASHITA, YOSHIATSU TANAKA, SHAJEDUL ISLAM, TAKAO KITAGAWA, KAZUHIRO TOKUDA, DURGA PAUDEL, SARITA GIRI, TOHRU OHTA, FUMIYA HARADA, HIROKI NAGAYASU, YASUHIRO KURAMITSU
Anticancer Research Nov 2025, 45 (11) 4743-4749; DOI: 10.21873/anticanres.17823

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DDX39 Is Down-regulated in Chromophobe Renal Cell Carcinoma Tissues, Whereas Overexpression Is Associated With Shorter Patient Survival
SHIN-NOSUKE YAMASHITA, YOSHIATSU TANAKA, SHAJEDUL ISLAM, TAKAO KITAGAWA, KAZUHIRO TOKUDA, DURGA PAUDEL, SARITA GIRI, TOHRU OHTA, FUMIYA HARADA, HIROKI NAGAYASU, YASUHIRO KURAMITSU
Anticancer Research Nov 2025, 45 (11) 4743-4749; DOI: 10.21873/anticanres.17823
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Keywords

  • DDX39
  • chromophobe renal cell carcinoma
  • clear cell renal cell carcinoma
  • papillary renal cell carcinoma
  • TCGA
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