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TBX3 promotes the epithelial mesenchymal transition of cervical cancer by upregulating ID1.

ABSTRACT: In this study, we aim to investigate the role and mechanism of T-box transcription factor 3 (TBX3) in cervical cancer. The mRNA and protein expression of TBX3, inhibitor of DNA binding 1 (ID1), and epithelial mesenchymal transition (EMT) markers (E-Cadherin, N-Cadherin, and vimentin) were measured using qRT-PCR and Western blot. shTBX3 and shID1 were transfected into SiHa cells to knockdown TBX3 and ID1. The metastasis and invasion abilities of cervical cancer cells were determined using a wound healing assay and an invasive assay. The shTBX3- and shID1-transfected SiHa cells were injected into nude mice using a xenograft tumor growth model. We found that TBX3 and ID1 were highly expressed in cervical cancer cells. Importantly, silencing TBX3 and ID1 significantly reduced the migration and metastasis of cervical cancer cells. In addition, silencing TBX3 and ID1 significantly inhibited the EMT, evidenced by the increased E-cadherin, and decreased N-cadherin and vimentin. The size and weight of the xenograft tumor were significantly reduced by shTBX3 and shID1. We demonstrate that TBX3 or ID1 knockdown can effectively inhibit cervical cancer cells migration and invasion. These findings indicate that TBX3 and ID1 can act as potential therapeutic targets for the prevention and treatment of cervical cancer.

SUBMITTER: Yang H

PROVIDER: S-EPMC10560953 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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TBX3 promotes the epithelial mesenchymal transition of cervical cancer by upregulating ID1.

Yang Hongyu H Sun Yanan Y Jia Xiaopeng X Cai Yuru Y Zhao Xingnan X Li Nan N

American journal of cancer research 20230915 9

In this study, we aim to investigate the role and mechanism of T-box transcription factor 3 (TBX3) in cervical cancer. The mRNA and protein expression of TBX3, inhibitor of DNA binding 1 (ID1), and epithelial mesenchymal transition (EMT) markers (E-Cadherin, N-Cadherin, and vimentin) were measured using qRT-PCR and Western blot. shTBX3 and shID1 were transfected into SiHa cells to knockdown TBX3 and ID1. The metastasis and invasion abilities of cervical cancer cells were determined using a wound ...[more]

PMID: 37818083

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Project description:ObjectiveTo explore the role of vasohibin-2 (VASH2) in regulation of proliferation and metastasis of cervical cancer cells.MethodsWe analyzed the differentially expressed genes between cervical cancer cells with flotillin-1 overexpression and knockdown by RNA-seq combined with analysis of public databases. The expression levels of VASH2 were examined in normal cervical epithelial cells (HcerEpic), cervical cancer cell lines (HeLa, C-33A, Ca ski, SiHa and MS751) and fresh cervical cancer tissues with different lymph node metastasis status. We further tested the effects of lentivirus-mediated overexpression and interference of VASH2 on proliferation, migration, invasion and lymphatic vessel formation of the cervical cancer cells and detected the expression levels of key epithelial-mesenchymal transition (EMT) markers and TGF-β mRNA.ResultsRNA-seq and analysis of public databases showed that VASH2 expression was significantly upregulated in cervical cancer cells exogenously overexpressing flotillin-1 (P < 0.05) and downregulated in cells with flotillin-1 knockdown (P < 0.05), and was significantly higher in cervical cancer tissues with lymph node metastasis than in those without lymph node metastasis (P < 0.01). In cervical cancer cell lines Ca Ski, SiHa, and MS751 and cervical cancer tissue specimens with lymph node metastasis, VASH2 expression was also significantly upregulated as compared with HcerEpic cells and cervical cancer tissues without lymph node metastasis (P < 0.05). Exogenous overexpression of VASH2 significantly promoted proliferation, migration, invasion and lymphatic vessel formation of cervical cancer cells, whereas these abilities were significantly inhibited in cells with VASH2 knockdown (P < 0.05). The cervical cancer cells overexpressing VASH2 showed significant down- regulation of e-cadherin and up- regulation of N-cadherin, Vimentin and VEGF-C, while the reverse changes were detected in cells with VASH2 knockdown (P < 0.05). TGF-β mRNA expression was significantly up-regulated in cervical cancer cells overexpressing VASH2 and down-regulated in cells with VASH2 knockdown (P < 0.001).ConclusionFlotillin-1 may participate in TGF-β signaling pathway-mediated EMT through its down-stream target gene VASH2 to promote the proliferation, migration, invasion and lymphatic vessel formation of cervical cancer cells in vitro.

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TBX3 promotes the epithelial mesenchymal transition of cervical cancer by upregulating ID1.

Publications

TBX3 promotes the epithelial mesenchymal transition of cervical cancer by upregulating ID1.

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