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胎盘特异性蛋白 1 促进非小细胞肺癌细胞的增殖和侵袭。

Placenta-specific protein 1 promotes cell proliferation and invasion in non-small cell lung cancer.

机构信息

Department of Oncology, First Affiliated Hospital, Nanjing Medical University, Gulou, Nanjing, Jiangsu 210029, P.R. China.

Department of Digestive, First Affiliated Hospital, Nanjing Medical University, Gulou, Nanjing, Jiangsu 210029, P.R. China.

出版信息

Oncol Rep. 2018 Jan;39(1):53-60. doi: 10.3892/or.2017.6086. Epub 2017 Nov 9.

Abstract

Pulmonary carcinoma-associated proteins have emerged as crucial players in governing fundamental biological processes such as cell proliferation, apoptosis and metastasis in human cancers. Placenta-specific protein 1 (PLAC1) is a cancer-related protein, which is activated and upregulated in a variety of malignant tissues, including prostate cancer, gastric adenocarcinoma, colorectal, epithelial ovarian and breast cancer. However, its biological role and clinical significance in non-small cell lung cancer (NSCLC) development and progression are still unknown. In the present study, we found that PLAC1 was significantly upregulated in NSCLC tissues, and its expression level was associated with advanced pathological stage and it was also correlated with shorter progression-free survival of lung cancer patients. Furthermore, knockdown of PLAC1 expression by siRNA inhibited cell proliferation, induced apoptosis and impaired invasive ability in NSCLC cells partly via regulation of epithelial-mesenchymal transition (EMT)-related protein expression. Our findings present that increased PLAC1 could be identified as a negative prognostic biomarker in NSCLC and regulate cell proliferation and invasion. Thus, we conclusively demonstrated that PLAC1 plays a key role in NSCLC development and progression, which may provide novel insights on the function of tumor-related gene-driven tumorigenesis.

摘要

肺癌相关蛋白已成为调控人类癌症中细胞增殖、凋亡和转移等基本生物学过程的关键因素。胎盘特异性蛋白 1(PLAC1)是一种与癌症相关的蛋白,在包括前列腺癌、胃腺癌、结直肠癌、上皮性卵巢癌和乳腺癌在内的多种恶性组织中被激活和上调。然而,其在非小细胞肺癌(NSCLC)发生和发展中的生物学作用及其临床意义尚不清楚。在本研究中,我们发现 PLAC1 在 NSCLC 组织中显著上调,其表达水平与晚期病理分期相关,并且与肺癌患者的无进展生存期缩短相关。此外,通过 siRNA 敲低 PLAC1 的表达抑制了 NSCLC 细胞的增殖,诱导了细胞凋亡,并部分通过调节上皮-间充质转化(EMT)相关蛋白的表达损害了细胞的侵袭能力。我们的研究结果表明,PLAC1 的增加可被视为 NSCLC 的负预后生物标志物,并调节细胞增殖和侵袭。因此,我们明确证明 PLAC1 在 NSCLC 的发生和发展中起着关键作用,这可能为肿瘤相关基因驱动的肿瘤发生的功能提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c6c/5783604/c4a4a6c9db5d/OR-39-01-0053-g00.jpg

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