A study on communication mechanism of lung cancer cells in tumor microenvironment mediated by pleckstrin-2/miR-196a signal axis

Autor: WANG Manli, CHEN Hui, DUAN Zhi, XU Qimei, LI Zhen
Jazyk: English<br />Chinese
Rok vydání: 2024
Předmět:
Zdroj: Zhongguo aizheng zazhi, Vol 34, Iss 7, Pp 628-638 (2024)
Druh dokumentu: article
ISSN: 1007-3639
DOI: 10.19401/j.cnki.1007-3639.2024.07.002
Popis: Background and purpose: It is still a great challenge to clarify the signal molecules that mediate the communication between cancer-associated fibroblasts (CAFs) and tumor cells. These signal molecules are very important for cancer metastasis. The purpose of this study was to explore the communication mechanism of pleckstrin-2/miR-196a signal axis mediated by lung cancer cells in tumor microenvironment. Methods: Human lung adenocarcinoma cell line H1299 and human embryonic lung cell MRC-5 were selected as the research objects. H1299 cells were transfected with lentivirus (PLEK2) expressing PLEK2 and Vector control, and exosomes (Vector_exo, PLEK2_exo) were isolated after 24 h of transfection. MRC-5 cells were transfected with miR-196a mimetic or inhibitor. The expressions of PLEK2 and epithelial-mesenchymal transition (EMT)-related proteins were analyzed by Western blot. The expression of miR-196a was analyzed by polymerase chain reaction (PCR), and the metastasis and invasion ability of cells were determined by transwell assay. Six female BALB/c-nu mice were randomly divided into Vector group and PLEK2 group, with 3 mice in each group. Mice in each group were injected with H1299 cells transfected with Vector or PLEK2 through the tail vein. After 4 weeks, lung tissue was taken out for H-E staining and immunohistochemical staining to analyze the expression of α-smooth muscle actin (α-SMA). All animal experiments were approved by the ethics committee of First Hospital of Changsha City (Changsha Hospital, Xiangya School of Medicine, Central South University) (ethics number: EI-2021-103). Results: Compared with the Vector group, the number of pulmonary metastatic nodules and the expression of α-SMA in metastatic cancer in PLEK2 group increased significantly (P
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