溶质载体家族16成员13（SLC16A13）下调促进A549肺癌细胞系的凋亡诱导
SLC16A13 Downregulation Contributes to Apoptosis Induction in A549 Lung Cancer Cell Line.
作者信息
Zeinolabedini Aysan, Zarredar Habib, Zafari Venus, Soleimani Zahra, Sabbagh-Jadid Hamed, Raeisi Mortaza
机构信息
Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of basic oncology of health institute of Ege University, Izmir, Turkey.
出版信息
Asian Pac J Cancer Prev. 2025 Feb 1;26(2):525-532. doi: 10.31557/APJCP.2025.26.2.525.
BACKGROUND
Lung cancer, a lethal type of malignancy in the world, has different pathological subcategories, among which NSCLC is the most common form. The complex pathogenesis of this disease has caused its treatment in advanced stages to be accompanied by many problems. Recently, the genes involved in metabolism, especially those coding for membrane transporter proteins (the solute carrier) have received attention in cancer studies. The Solute Carrier Family 16 Member 1 (SLC16A) is membrane transporters the role of which in the promotion of cancer has been revealed in recent years. This study aimed to examine the effect of SLC16A13 low expression in A549 lung cancer cells, focusing on its role in key cellular processes such as viability, proliferation, and apoptosis. By targeting SLC16A13, a critical member of the solute carrier family implicated in cancer metabolism, the study search for to uncover molecular mechanisms that could inform novel therapeutic strategies for non-small cell lung cancer.
METHODS
At first, the A549 lung cancer cell line was cultured in a standard medium, and then specific synthetic SLC16A13 sh-RNA was transfected into the A549 cell line to suppress the expression of this membrane transporter. We used MTT and flow cytometry tests to investigate the effect of reducing the expression of SLC16A13 on the process of cell viability and apoptosis. Also, the change of gene expression was analyzed by Real-Time PCR.
RESULTS
In the present study, the reduction of SLC16A13 gene expression caused an increase in the apoptosis rate and reduced cell viability in lung cancer cells. Also, SLC16A13 suppression may induce apoptosis pathway by upregulating Bax, Caspase-3, and Caspase-9 expression while downregulation Bcl-2 expression. Besides, it was shown that SLC16A13 downregulation couldn't affect E-cadherin expression.
CONCLUSION
SLC16A13 may a promising target to increase cell death in lung cancer cells by inducing apoptosis pathways.
背景
肺癌是全球致死性的恶性肿瘤类型，有不同的病理亚类，其中非小细胞肺癌（NSCLC）是最常见的形式。该疾病复杂的发病机制导致其晚期治疗伴随诸多问题。近年来，参与代谢的基因，尤其是编码膜转运蛋白（溶质载体）的基因在癌症研究中受到关注。溶质载体家族16成员1（SLC16A）是膜转运蛋白，其在癌症促进中的作用近年来已被揭示。本研究旨在检测SLC16A13低表达在A549肺癌细胞中的作用，重点关注其在细胞活力、增殖和凋亡等关键细胞过程中的作用。通过靶向溶质载体家族中与癌症代谢相关的关键成员SLC16A13，本研究试图揭示可能为非小细胞肺癌新治疗策略提供依据的分子机制。
方法
首先，将A549肺癌细胞系培养于标准培养基中，然后将特异性合成的SLC16A13 sh-RNA转染至A549细胞系以抑制该膜转运蛋白的表达。我们使用MTT和流式细胞术检测来研究降低SLC16A13表达对细胞活力和凋亡过程的影响。此外，通过实时定量PCR分析基因表达的变化。
结果
在本研究中，SLC16A13基因表达的降低导致肺癌细胞凋亡率增加和细胞活力降低。此外，SLC16A13的抑制可能通过上调Bax、Caspase-3和Caspase-9的表达，同时下调Bcl-2的表达来诱导凋亡途径。此外，研究表明SLC16A13的下调不影响E-钙黏蛋白的表达。
结论
SLC16A13可能是通过诱导凋亡途径增加肺癌细胞死亡的一个有前景的靶点。
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