PT  - JOURNAL ARTICLE
AU  - KITAGAWA, TAKAO
AU  - ISLAM, SHAJEDUL
AU  - BARON, BYRON
AU  - TOKUDA, KAZUHIRO
AU  - PAUDEL, DURGA
AU  - OHTA, TOHRU
AU  - NAKAGAWA, KOJI
AU  - KOBAYASHI, MASANOBU
AU  - OKADA, FUTOSHI
AU  - KURAMITSU, YASUHIRO
TI  - A Standardized Extract of Cultured <em>Lentinula edodes mycelia</em> Up-regulates COX-2 in Inflammation-related Malignant Progressive Fibrosarcoma Cell Clone QRsP-11
AID  - 10.21873/anticanres.16270
DP  - 2023 Mar 01
TA  - Anticancer Research
PG  - 1239--1244
VI  - 43
IP  - 3
4099  - http://ar.iiarjournals.org/content/43/3/1239.short
4100  - http://ar.iiarjournals.org/content/43/3/1239.full
SO  - Anticancer Res2023 Mar 01; 43
AB  - Background/Aim: Cyclooxygenase is an enzyme that transforms arachidonic acid to prostaglandins. Cyclooxygenase-2 (COX-2) is an isoform of cyclooxygenase. There exist many reports on the expression levels of COX-2 in cancer tissues, and prognosis of cancer patients has been reported to be related to COX-2 up-regulation. In the present study we assessed the suppressive effect of AHCC® on the expression of COX-2 in QRsP-11cells. Materials and Methods: QR-32 is a clone which was derived from murine fibrosarcoma BMT-11 cells by treatment with quercetin. These clone cells regress spontaneously after injection into C57BL/6 mice. QRsP-11 is a clone derived from QR-32, showing very aggressive tumorigenicity. AHCC® is a standardized extract of cultured Lentinula edodes mycelia and has been reported to exert suppressive effects on various tumor-associated proteins including HSP27. The protein levels of COX-2 in QR-32 and QRsP-11 cells were compared by using western blotting. Furthermore, the expression levels of COX-2 were assessed in QRsP-11 cells after AHCC®-treatment. Results: Western blot analysis showed a significant up-regulation of COX-2 in QRsP-11 cells compared to QR-32 cells. In vitro AHCC®-treatment increased COX-2 expression levels in QRsP-11 cells contrary to expectations. Conclusion: When using AHCC® in cancer treatment, it might be important to decrease COX-2 expression by means of non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin. Further studies are required to clarify the mechanism of up-regulation of COX-2 through AHCC®-treatment.