PDF(Pubmed)
Abstract：
OBJECTIVE: Non-small-cell lung cancer (NSCLC) is a deadly form of cancer that exhibits extensive intercellular communication which contributed to chemoradiotherapy resistance. Recent evidence suggests that arrange of key proteins are involved in lung cancer progression, including gap junction proteins (GJPs).
RESULTS: In this study, we examined the expression patterns of GJPs in NSCLC, uncovering that both gap junction protein, beta 2 (GJB2) and gap junction protein, beta 2 (GJB3) are increased in LUAD and LUSC. We observed a correlation between the upregulation of GJB2, GJB3 in clinical samples and a worse prognosis in patients with NSCLC. By examining the mechanics, we additionally discovered that nuclear factor erythroid-2-related factor 1 (NFE2L1) had the capability to enhance the expression of connexin26 and connexin 31 in the NSCLC cell line A549. In addition, the use of metformin was discovered to cause significant downregulation of gap junction protein, betas (GJBs) by limiting the presence of NFE2L1 in the cytoplasm.
CONCLUSIONS: This emphasizes the potential of targeting GJBs as a viable treatment approach for NSCLC patients receiving metformin.
RESULTS: In this study, we examined the expression patterns of GJPs in NSCLC, uncovering that both gap junction protein, beta 2 (GJB2) and gap junction protein, beta 2 (GJB3) are increased in LUAD and LUSC. We observed a correlation between the upregulation of GJB2, GJB3 in clinical samples and a worse prognosis in patients with NSCLC. By examining the mechanics, we additionally discovered that nuclear factor erythroid-2-related factor 1 (NFE2L1) had the capability to enhance the expression of connexin26 and connexin 31 in the NSCLC cell line A549. In addition, the use of metformin was discovered to cause significant downregulation of gap junction protein, betas (GJBs) by limiting the presence of NFE2L1 in the cytoplasm.
CONCLUSIONS: This emphasizes the potential of targeting GJBs as a viable treatment approach for NSCLC patients receiving metformin.
摘要：
目的：非小细胞肺癌（NSCLC）是一种致命的癌症形式，表现出广泛的细胞间通讯，导致放化疗耐药。最近的证据表明，关键蛋白的排列与肺癌的进展有关。包括间隙连接蛋白(GJPs)。
结果：在这项研究中，我们检查了非小细胞肺癌中GJPs的表达模式，发现两种间隙连接蛋白，β2（GJB2）和缝隙连接蛋白，β2（GJB3）在LUAD和LUSC中增加。我们观察到临床样本中GJB2，GJB3的上调与NSCLC患者预后较差之间存在相关性。通过检查力学，我们还发现核因子红系-2相关因子1(NFE2L1)能够增强NSCLC细胞系A549中连接蛋白26和连接蛋白31的表达.此外,二甲双胍的使用被发现导致间隙连接蛋白的显著下调，β（GJBs）通过限制NFE2L1在细胞质中的存在。
结论：这强调了靶向GJBs作为接受二甲双胍的NSCLC患者的可行治疗方法的潜力。
结果：在这项研究中，我们检查了非小细胞肺癌中GJPs的表达模式，发现两种间隙连接蛋白，β2（GJB2）和缝隙连接蛋白，β2（GJB3）在LUAD和LUSC中增加。我们观察到临床样本中GJB2，GJB3的上调与NSCLC患者预后较差之间存在相关性。通过检查力学，我们还发现核因子红系-2相关因子1(NFE2L1)能够增强NSCLC细胞系A549中连接蛋白26和连接蛋白31的表达.此外,二甲双胍的使用被发现导致间隙连接蛋白的显著下调，β（GJBs）通过限制NFE2L1在细胞质中的存在。
结论：这强调了靶向GJBs作为接受二甲双胍的NSCLC患者的可行治疗方法的潜力。
