Laminin γ-2 (LAMC2) promotes the proliferation and invasion of pancreatic cancer cells by regulating PI3K/Akt signaling

IF 0.9 Q4 GASTROENTEROLOGY & HEPATOLOGY Journal of Pancreatology Pub Date : 2024-01-09 DOI:10.1097/jp9.0000000000000166
Qi Wang, Fusheng Zhang, Di Long, Weikang Liu, Yiran Chen, Yongsu Ma, Yinmo Yang, Zebin Mao, Xiaodong Tian
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Abstract

Pancreatic ductal adenocarcinoma (PDAC) poses a serious threat to human health with high mortality and poor prognosis, and there is an urgent need to explore the pathogenesis of PDAC in order to search for new therapeutic targets. The expression of LAMC2 in PDAC and its effect on the prognosis of tumor patients were predicted by an online database, and the expression level of LAMC2 in pancreatic cancer was verified by PCR and western blot; flow cytometry, wound healing assay, CCK8 assay, and colony formation assay were used to explore the effect of LAMC2 on the proliferation and migration of pancreatic cancer cells; and we also probed the potential relationship between LAMC2 and PI3K/Akt signaling. High levels of LAMC2 in pancreatic cancer may benefit tumor proliferation migration and invasion and lead to poor prognosis of tumor patients. And the mechanism by which LAMC2 promotes PDAC progression may be related to the activation of PI3K/Akt signaling to influence apoptosis, cell cycle. LAMC2 promotes proliferation migration invasion of PDAC and leads to poor prognosis in pancreatic cancer patients.
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层粘蛋白γ-2(LAMC2)通过调节 PI3K/Akt 信号促进胰腺癌细胞的增殖和侵袭
胰腺导管腺癌(PDAC)死亡率高、预后差,严重威胁人类健康,迫切需要探索PDAC的发病机制,以寻找新的治疗靶点。 我们通过在线数据库预测了LAMC2在PDAC中的表达及其对肿瘤患者预后的影响,并通过PCR和Western blot验证了LAMC2在胰腺癌中的表达水平;利用流式细胞术、伤口愈合试验、CCK8试验和集落形成试验探讨了LAMC2对胰腺癌细胞增殖和迁移的影响;我们还探究了LAMC2与PI3K/Akt信号转导之间的潜在关系。 胰腺癌中高水平的LAMC2可能有利于肿瘤的增殖迁移和侵袭,并导致肿瘤患者预后不良。而LAMC2促进PDAC进展的机制可能与激活PI3K/Akt信号转导影响细胞凋亡、细胞周期有关。 LAMC2促进了PDAC的增殖迁移和侵袭,并导致胰腺癌患者预后不良。
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Laminin γ-2 (LAMC2) promotes the proliferation and invasion of pancreatic cancer cells by regulating PI3K/Akt signaling
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