2020
DOI: 10.12659/msm.918123
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Downregulation of SEMA4C Inhibit Epithelial-Mesenchymal Transition (EMT) and the Invasion and Metastasis of Cervical Cancer Cells via Inhibiting Transforming Growth Factor-beta 1 (TGF-β1)-Induced Hela cells p38 Mitogen-Activated Protein Kinase (MAPK) Activation

Abstract: Background: Epithelial-mesenchymal transition (EMT) plays a key role in promoting invasion and metastasis of tumor cells. SEMA4C can regulate the generation of transforming growth factor-beta 1 (TGF-b1)-induced EMT in cervical cancer. This study investigated the relationship between the regulation of SEMA4C on TGF-b1-induced p38 mitogen-activated protein kinase (MAPK) activation and invasion and metastasis of cervical cancer. Material/Methods: Hela-shSEMA4C cell line was established and the success of transfec… Show more

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Cited by 17 publications
(16 citation statements)
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“…Xue et al have already described the contribution of Akt activation in the process of EMT [ 90 ]. In contrast, p38 MAPK activation possess an EMT promoting role [ 91 , 92 ]. Our results showed increased activation status of p38 MAPK in all treated groups.…”
Section: Discussionmentioning
confidence: 99%
“…Xue et al have already described the contribution of Akt activation in the process of EMT [ 90 ]. In contrast, p38 MAPK activation possess an EMT promoting role [ 91 , 92 ]. Our results showed increased activation status of p38 MAPK in all treated groups.…”
Section: Discussionmentioning
confidence: 99%
“…EMT is reported to be an important cause of distal metastases of malignant tumors ( 37 ). Accumulating evidence has demonstrated that metastatic potential can be enhanced by activating EMT in numerous types of cancer, including HCC ( 38 ), BC ( 39 ) and cervical cancer ( 40 ). The present study revealed that overexpression of PFKP decreased the protein expression levels of E-cadherin, and increased the protein expression levels of N-cadherin and vimentin, whereas knockdown of PFKP had the opposite effect.…”
Section: Discussionmentioning
confidence: 99%
“…In recent years, studies on malignant tumors have revealed that TGF-β1 and TGF-βR1 may serve important roles in tumor occurrence and development, including in promoting tumor angiogenesis, invasion, EMT and immune escape ( 4 , 5 , 197 ). Increased expression levels of miR-331-3p ( 22 ), HnRNP K ( 146 ), Sema4C ( 157 ) and p68 ( 156 ), and the activation of the JAK/STAT3/Twist ( 111 ), NF-κB ( 127 ) and TGF-β signaling pathways in tumor cells can promote proliferation, migration and EMT through the action of TGF-β1 or TGF-βR1. Increased levels of some molecules, such as miR-133b ( 63 ), miR-4458 and miR-27a ( 168 ), inhibit the progression of tumors by acting on TGF-β1 or TGF-βR1.…”
Section: Discussionmentioning
confidence: 99%
“…TGF-β1 can regulate the development of EMT and is considered to be the driving force of EMT in cervical cancer ( 156 ). Yang et al ( 157 ) reported that semaphorin 4C (Sema4C) downregulation inhibited cervical cancer cell EMT, invasion and metastasis, possibly by inhibiting TGF-β1-induced activation of p38 MAPK in HeLa cells. However, Li et al ( 156 ) found that p68 promoted EMT in cervical cancer cells through transcriptional activation of the TGF-β1 signaling pathway.…”
Section: Tgf-β Tgf-βr1 and Malignant Tumorsmentioning
confidence: 99%