<p>LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT</p>

Abstract

Purpose: Gastric cancer (GC) is the fifth most common tumor in the world, and most patients with GC have a poor prognosis. This study aimed to explore the biological influence and mechanism of LINC01272 in GC. Materials and Methods: Using bioinformatic analyses, we investigated the expression of LINC01272 in TCGA database and predicted the biological functions and mechanism of LINC01272 in GC. Then, we detected the expression of LINC01272 in GC cell lines, GC tissues, and corresponding normal tissues using real-time polymerase chain reaction (RT-PCR). Finally, we explored the migration and invasion ability of LINC01272 by wound-healing and Transwell assays and examined the expression of epithelial-mesenchymal transition (EMT)related proteins through Western blotting. Results: We found that LINC01272 was upregulated in GC and was associated with GC staging and lymph node metastasis. The results of wound-healing and Transwell assays revealed that the LINC01272 was closely related to GC cell migration and invasion. LINC01272 knockdown inhibited the migration and invasion ability of GC cells by reducing the expression of EMT-related proteins. Overexpression of LINC01272 had the opposite effect. Conclusion: Together, our results showed that LINC01272 promoted GC metastasis ability by regulating the expression of EMT-related proteins and could serve as a potential diagnostic biomarker for GC.

Effect and mechanism of downregulating the long-chain noncoding RNA TM4SF1-AS1 on the proliferation, apoptosis and invasion of gastric cancer cells

“…Studies have shown that the EMT is closely related to the high invasion and metastasis of carcinoma cells [ 22 , 23 ]. An increasing amount of evidence has revealed that lncRNAs participate in the occurrence and progression of carcinoma by regulating the EMT of carcinoma cells, play the role of oncogene promoters or tumour suppressors and become key regulators of the migration, invasion and metastasis of tumour cells [ 24 ]. After downregulating and silencing lncTM4SF1-AS1, the expression levels of the E-cadherin protein, a marker protein of epithelial properties, were significantly increased, while the levels of N-cadherin, Snail and Twist 1 protein related to mesothelial properties were significantly decreased during the EMT.…”

Identification of a nine ferroptosis-related lncRNA prognostic signature for lung adenocarcinoma

“…LINC01116 has been studied as an oncogene in many tumors, such as LAUD, its overexpression promotes LAUD proliferation and metastasis [53], contributes to ge tinib resistance in NSCLS through regulating IFI44 [54], results in resistance of LAUD to cisplatin via the EMT process [55]. Leng X et al indicated that SMIM25 (Aliases LINC01272) promoted gastric cancer metastasis through regulating EMT process [56]. The remaining lncRNAs have not seen relevant reports in previous studies, which are worthy of further research.…”

LINC01018 and SMIM25 sponged miR-182-5p in endometriosis revealed by the ceRNA network construction

“…The SMIM25, also known as LINC01272, was upregulated gastric cancer (GC), and the over-expression of SMIM25 promoted the migration and invasion ability of GC cells by activating the epithelial-mesenchymal transition (EMT) process. 26 The EMT defines a process by which epithelial cells lose their cell polarity and cell-to-cell adhesion and acquire the migratory and invasive properties to become mesenchymal cells. 27 These changes are supposed to contribute to the establishment of endometriotic lesions in Ems.…”