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Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
Published on: February 16, 2024
LINC02535 promotes cell growth in poorly differentiated gastric cancer
Jianzhong Wu1,2, Ling Gao1, Hong Chen1
1Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Background:
Abnormal long non-coding RNA (lncRNA) expression plays important roles in gastric cancer. However, the functions of many lncRNAs in poorly differentiated gastric cancer (PDGC) remain unknown.
Methods:
Three sets of paired tissues from patients with PDGC were used, and transcriptome sequencing was performed, followed by the construction and sequencing of a library and mapping of the reads. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and protein-protein interaction (PPI) networks were analysed, and canonical pathway significance was calculated among the differentially expressed genes (DEGs; p < 0.05). Gene expression in 30 paired PDGC specimens and four cell lines was validated through quantitative PCR. Cell proliferation, migration, invasion, apoptosis, and wound healing were analysed.
Results:
A total of 499 upregulated DEGs and 627 downregulated DEGs were identified between peritumoral and gastric cancer tissues. The proportions of positive and negative correlations between LINC02535 and the DEGs were 98.40% and 92.66%, respectively, while the Spearman's correlation coefficient was greater than 0.5. The PPI network showed that approximately 73.15% of the top five genes were directly correlated with LINC02535 according to the STRING database. Based on KEGG analysis, the functions of LINC02535 target genes were enriched in signalling pathways related to cancer cell growth. Furthermore, cell function studies showed that LINC02535 upregulation contributed to cell proliferation, migration, invasion, and wound healing and that its inhibition facilitated cell apoptosis.
Conclusion:
LINC02535 expression was upregulated in PDGC and contributed to cell proliferation, migration, invasion and wound healing, whereas its inhibition in PDGC facilitated cell apoptosis.
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