ArticleExperimental and therapeutic medicine2022
Pseudogene CSPG4P12 affects the biological behavior of non‑small cell lung cancer by Bcl‑2/Bax mitochondrial apoptosis pathway.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Machine learning-based identification of small RNA signatures in aqueous humor as a step toward precision diagnosis of glaucoma.Annals of medicine · 2025Article
- CSPG4P12 polymorphism served as a susceptibility marker for esophageal cancer in Chinese population.BMC cancer · 2024Article
- Pseudogene CSPG4P12 inhibits colorectal cancer progression by attenuating epithelial-mesenchymal transition.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
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Authors and funding
7 authors.
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Abstract
Increasing evidence has shown that chondroitin sulfate proteoglycan 4 (CSPG4) serve a critical role in tumor progression. However, the roles of chondroitin sulfate proteoglycan 4 pseudogene 12 (CSPG4P12) remain to be elucidated. The present study aimed to investigate the potential effects of CSPG4P12 on the physiological behaviors of non-small cell lung cancer (NSCLC) and its underlying biological mechanism. The expression levels of CSPG4P12 in NSCLC tissues and adjacent normal tissues were analyzed using the gene expression profiling interactive analysis 2 database and reverse transcription-quantitative PCR. Cell Counting Kit-8 and colony formation assays were performed to measure cell proliferation. In addition, Transwell and wound healing assays were performed to assess cell invasion and migration. Cell adhesion was measured by cell-extracellular matrix adhesion assay. Hoechst 33342 staining assay was performed to detect nucleoli of apoptotic cells, and transmission electron microscopy (TEM) was utilized for apoptosis detection. Immunofluorescence and western blot assays were performed to measure the expression levels of apoptosis-related proteins. The present results revealed that the expression levels of CSPG4P12 in NSCLC tissues were significantly lower compared with those in adjacent normal tissues. Overexpression of CSPG4P12 inhibited cell proliferation, invasion, migration and adhesion whilst promoting apoptosis. There were missing mitochondrial cristae and mitochondrial vacuoles in the CSPG4P12-overexpressed cells when observed under TEM. Overexpression of CSPG4P12 also increased the expression of Bax and p53, whereas it inhibited the expression of Bcl2. In conclusion, CSPG4P12 could inhibit NSCLC development and tumorigenesis by activating the p53/Bcl2/Bax mitochondrial apoptotic pathway.
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