PT  - JOURNAL ARTICLE
AU  - MD RASHEDUNNABI AKANDA
AU  - JEE SOO PARK
AU  - MYUNG-GIUN NOH
AU  - GEUN-HYOUNG HA
AU  - YOUNG SOOK PARK
AU  - JAE-HYUK LEE
AU  - KYUNG-SUB MOON
AU  - CHUNG KWON KIM
AU  - KYUNG-HWA LEE
TI  - TACC3 Promotes Gastric Carcinogenesis by Promoting Epithelial-mesenchymal Transition Through the ERK/Akt/cyclin D1 Signaling Pathway
AID  - 10.21873/anticanres.15123
DP  - 2021 Jul 01
TA  - Anticancer Research
PG  - 3349--3361
VI  - 41
IP  - 7
4099  - http://ar.iiarjournals.org/content/41/7/3349.short
4100  - http://ar.iiarjournals.org/content/41/7/3349.full
SO  - Anticancer Res2021 Jul 01; 41
AB  - Background/Aim: The present study investigated the oncogenic functions of TACC3 in the progression of gastric cancer (GC). Materials and Methods: We analysed TACC3 in relation to cell growth, invasion capability, expression of epithelial-mesenchymal transition (EMT)-related markers, and ERK/Akt/cyclin D1 signaling factors. The correlation between the immunohistochemically confirmed expression of TACC3 and clinical factors was also analyzed. Results: The increased proliferation and invasion of TACC3-over-expressing GC cells was accompanied by altered regulation of EMT-associated markers and activation of ERK/Akt/cyclin D1 signaling. Immunohistochemical analysis of TACC3 in human GC tissues revealed that its expression is correlated with aggressive characteristics and poor prognosis of intestinal-type GC. Conclusion: TACC3 contributes to gastric tumorigenesis by promoting EMT via the ERK/Akt/cyclin D1 signaling pathway. The correlation between TACC3 expression and multiple clinicopathological variables implies that its effective therapeutic targeting in GC will depend on the tumor subtype.