CSE1L, as a novel prognostic marker, promotes pancreatic cancer proliferation by regulating the AKT/mTOR signaling pathway.
CSE1L, as a novel prognostic marker, promotes pancreatic cancer proliferation by regulating the AKT/mTOR signaling pathway.
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CSE1L作为一种新型预后标志物，通过调节AKT/mTOR信号通路促进胰腺癌增殖
DOI：
10.7150/jca.54482
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发表时间：
2021
影响因子：
3.9
通讯作者：
Wang L
中科院分区：
文献类型：
--
作者：
Zhang X;Zhang X;Mao T;Xu H;Cui J;Lin H;Wang L
胰腺癌是最具侵袭性的肿瘤之一，预后差，迫切需要新的靶向治疗。CSE1L（chromosome segregation 1 like）被认为在肿瘤发生中起重要作用，并作为癌症治疗靶点。然而，CSE1L在胰腺癌中的生物学功能和潜在机制仍不完全清楚。在本研究中，根据癌症基因组图谱（TCGA）数据库的数据，我们发现CSE1L高表达与胰腺癌患者的预后不良有关。此外，我们发现CSE1L敲低抑制胰腺癌细胞的增殖并促进凋亡，而CSE1L过表达则表现出相反的现象。此外，我们发现CSE 1L可能通过AKT信号通路调节胰腺癌的增殖。总之，我们揭示了CSE1L在肿瘤生长中起着至关重要的作用，并可能作为胰腺癌的潜在预后和治疗靶点。
Pancreatic cancer is one of the most aggressive tumors with poor prognosis and new targetable therapies are urgently required. CSE1L (chromosome segregation 1 like) is thought to play an important role in tumorigenesis and acts as a cancer therapeutic target. However, the biological function and the underlying mechanism of CSE1L in pancreatic cancer are still not fully explicit. In the present study, we found that high CSE1L expression was related to a worse prognosis in patients with pancreatic cancer according to data from the Cancer Genome Atlas (TCGA) database. Additionally, we found that CSE1L knockdown inhibited the proliferation of pancreatic cancer cells and promoted apoptosis, while CSE1L overexpression demonstrated the opposite phenomenon. Furthermore, we discovered that CSE1L might regulate pancreatic cancer proliferation through AKT signaling pathway. In summary, we reveal that CSE1L plays a crucial role in tumor growth and may serve as a potential prognostic and therapeutic target for pancreatic cancer.
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