Sorafenib-induced Aquaporin-3 Downregulation is Coupled With Proliferation Inhibition and Increased Apoptosis in Hepatocellular Carcinoma Cells
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TextPublisher number: Phone: +255 28 298 3384 Fax: +255 28 298 3386 Email: vc@bugando.ac.tz Website: www.bugando.ac.tz Language: English Original language: English Publication details: Mwanza, Tanzania: Research Square & Catholic University of Health and Allied Sciences [CUHAS – Bugando] 2020/12/9Description: Pages 1-19Online resources: Summary: Sorafenib is the only targeted therapy promising to improve the prognosis of patients with advanced hepatocellular carcinoma (HCC), but its long-term clinical e cacy is limited due to chemotherapy resistance. The lack of a full understanding of the anti-tumor mechanism of sorafenib in HCC is attributed to the di culties in understanding the mechanism of drug resistance. In recent years, a large number of preclinical and clinical data have con rmed the catalytic role of aquaporin-3 (AQP3) in a variety of tumors including HCC, but none of the studies reported the regulatory mechanism of AQP3 during sorafenib treatment. This study examined the effect of sorafenib on the expression of AQP3 in HCC cells and determined whether the effect is associated with cell proliferation inhibition, cell cycle arrest, and increased apoptotic.
| Item type | Current library | Collection | Copy number | Status | Barcode | |
|---|---|---|---|---|---|---|
| RESEARCH ARTICLES | MWALIMU NYERERE LEARNING RESOURCES CENTRE-CUHAS BUGANDO | NFIC | RA1097 | -1 | RA1097 |
Sorafenib is the only targeted therapy promising to improve the prognosis of patients with advanced hepatocellular carcinoma (HCC), but its long-term clinical e cacy is limited due to chemotherapy resistance. The lack of a full understanding of the anti-tumor mechanism of sorafenib in HCC is attributed to the di culties in understanding the mechanism of drug resistance. In recent years, a large number of preclinical and clinical data have con rmed the catalytic role of aquaporin-3 (AQP3) in a variety of tumors including HCC, but none of the studies reported the regulatory mechanism of AQP3 during sorafenib treatment. This study examined the effect of sorafenib on the expression of AQP3 in HCC cells and determined whether the effect is associated with cell proliferation inhibition, cell cycle arrest, and increased apoptotic.
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