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Claudin14 promotes colorectal cancer progression via the PI3K/AKT/mTOR pathway.
Neoplasma ( IF 2.0 ) Pub Date : 2021-06-23 , DOI: 10.4149/neo_2021_210210n203
Tian-Yu Qiao 1 , Zi-Ming Yuan 1 , Tian-Yi Ma 1 , Han-Qing Hu 1 , Yi-Hao Zhu 1 , Wei-Yuan Zhang 1 , Qian Zhang 1 , Rui Huang 1 , Qing-Chao Tang 1 , Gui-Yu Wang 2 , Xi-Shan Wang 1, 3
Affiliation  

Colorectal cancer is the third leading cancer in the world in terms of incidence and mortality. The role of differentially expressed Claudin14 (CLDN14) in CRC has not been reported. We observed that CLDN14 was associated with the progression of CRC. Our functional studies have shown that CLDN14 promoted the proliferation of CRC cells. In addition, and CLDN14 also increased the migration and invasion of CRC cells. In vivo experiments also showed that CLDN14 promoted the growth of colorectal cancer via the PI3K/AKT/mTOR. In summary, our research suggests that CLDN14 promotes the progression of colorectal cancer. Our findings may provide new strategies for clinical management and patient prognosis of CRC.

中文翻译:

Claudin14 通过 PI3K/AKT/mTOR 通路促进结直肠癌进展。

就发病率和死亡率而言,结直肠癌是世界第三大癌症。差异表达的 Claudin14 (CLDN14) 在 CRC 中的作用尚未见报道。我们观察到 CLDN14 与 CRC 的进展有关。我们的功能研究表明 CLDN14 促进了 CRC 细胞的增殖。此外,CLDN14还增加了CRC细胞的迁移和侵袭。体内实验还表明,CLDN14 通过 PI3K/AKT/mTOR 促进结直肠癌的生长。总之,我们的研究表明 CLDN14 促进了结直肠癌的进展。我们的发现可能为 CRC 的临床管理和患者预后提供新的策略。
更新日期:2021-06-24
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