TM9SF1 promotes bladder cancer cell growth and infiltration

Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To impr...

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Veröffentlicht in:World journal of clinical oncology 2024-02, Vol.15 (2), p.302-316
Hauptverfasser: Wei, Long, Wang, Shi-Shuo, Huang, Zhi-Guang, He, Rong-Quan, Luo, Jia-Yuan, Li, Bin, Cheng, Ji-Wen, Wu, Kun-Jun, Zhou, Yu-Hong, Liu, Shi, Li, Sheng-Hua, Chen, Gang
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Sprache:eng
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Zusammenfassung:Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To improve the survival rate and prognosis of BC patients, it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention. Transmembrane 9 superfamily member 1 (TM9SF1), also known as MP70 and HMP70, is a member of a family of nine transmembrane superfamily proteins, which was first identified in 1997. can be expressed in BC, but its biological function and mechanism in BC are not clear. To investigate the biological function and mechanism of in BC. Cells at 60%-80% confluence were transfected with lentiviral vectors for 48-72 h to achieve stable overexpression or silencing in three BC cell lines (5637, T24, and UM-UC-3). The effect of on the biological behavior of BC cells was then investigated through CCK8, wound-healing assay, transwell assay, and flow cytometry. Overexpression of increased the proliferation, migration, and invasion of BC cells by promoting the entry of BC cells into the G2/M phase. Silencing of inhibited proliferation, migration, and invasion of BC cells and blocked BC cells in the G1 phase. may be an oncogene in BC.
ISSN:2218-4333
2218-4333
DOI:10.5306/wjco.v15.i2.302