Long non-coding RNAs (lncRNAs) play crucial roles in many biological and pathological processes, including tumor metastasis. Here we reported a novel lncRNA, LINC01133 that was downregulated by TGF-β, which could inhibit epithelial-mesenchymal transition (EMT) and metastasis in colorectal cancer (CRC) cells. An alternative splicing factor SRSF6 was identified to directly interact with LINC01133, and SRSF6 promoted EMT and metastasis in CRC cells independent of LINC01133 And we confirmed that the EMT process was regulated by LINC01133 in CRC cells dependent on the presence of SRSF6. The observation for LINC01133 to inhibit metastasis was also verified in vivo. Moreover clinical data showed that the LINC01133 expression was positively correlated with E-cadherin, and negatively correlated with Vimentin, and there was a robust association of low LIINC01133 expression in tumors with poor survival in CRC samples. These data suggest that LINC01133 inhibits the EMT and metastasis by directly binding to SRSF6 as a target mimic, and may serve as a prognostic biomarker and an effective target for anti-metastasis therapies for CRC.
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http://dx.doi.org/10.1016/j.canlet.2016.07.015 | DOI Listing |
Int J Biol Sci
January 2025
The People's Hospital of Gaozhou, Gaozhou 525200, China.
Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant (-diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of General Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
The underlying mechanisms between cancer stem cells (CSC) and epithelial-mesenchymal transition (EMT) in pancreatic cancer (PC) remain unclear. In this study, we identified TGIF2 as a target gene of CSC using sncRNA and machine learning. TGIF2 is closely related to the expression of SOX2, EGFR, and E-cadherin, indicating poor prognosis.
View Article and Find Full Text PDFJ Mol Histol
January 2025
Department of Laboratory Medicine, Xiamen Key Laboratory of Genetic Testing, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55 Zhenhai Road, Siming District, Xiamen, 361003, Fujian, China.
Objective: This study aimed to elucidate the role of pyruvate dehydrogenase kinase-1 (PDK1) in cervical cancer (CC) by investigating its impact on cell proliferation, migration, and epithelial-mesenchymal transition (EMT) under hypoxic conditions.
Methods: PDK1-silenced CC cell lines were established using lentiviral shRNA technology. Cell migration and invasion were assessed through scratch and Transwell assays, respectively.
Small
January 2025
State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Capturing circulating tumor cells (CTCs) in vivo from the bloodstream lessens tumor metastasis and recurrence risks. However, the absence of CTC receptors due to epithelial-mesenchymal transition (EMT), the limited binding capacity of a single ligand, and the complexity of the blood flow environment significantly reduce the efficiency of CTC capture in vivo. Herein, a multivalent ligand-decorated microsphere enrichment system (MLMES) is crafted that incorporates a capture column replete with an immunosorbent that precisely recognizes and binds the stably expressed cluster of differentiation 44 (CD44) and glucose transporter protein 1 (GLUT1) receptors present on the exterior of CTCs.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Biology, College of Chemistry & Life Science, Beijing University of Technology, Chaoyang, Beijing, China.
Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, characterized by a high incidence in late stages, high mortality rate, and poor prognosis. Src Homology 2 Domain Containing Protein 5 (SH2D5) is a mammalian-specific, uncharacterized scaffolding protein, and its role in LUAD remains unclear. In the present study, we investigated the function and potential mechanisms of SH2D5 in the progression of LUAD.
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