Dataset Information

Kv3.4 regulates cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition in A549 cells.

ABSTRACT: Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. This process induces cell migration and invasion, which are closely related to cancer metastasis and malignancy. EMT consists of various intermediate states that express both epithelial and mesenchymal traits, called partial EMT. Recently, several studies have focused on the roles of voltage-gated potassium (Kv) channels associated with EMT in cancer cell migration and invasion. In this study, we demonstrate the relationship between Kv3.4 and EMT and confirm the effects of cell migration and invasion. With TGF-β treatment, EMT was induced and Kv3.4 was also increased in A549 cells, human lung carcinoma cells. The knockdown of Kv3.4 blocked the EMT progression reducing cell migration and invasion. However, the Kv3.4 overexpressed cells acquired mesenchymal characteristics and increased cell migration and invasion. The overexpression of Kv3.4 also has a synergistic effect with TGF-β in promoting cell migration. Therefore, we conclude that Kv3.4 regulates cancer migration and invasion through TGF-β-induced EMT and these results provide insights into the understanding of cancer metastasis.

SUBMITTER: Sim HJ

PROVIDER: S-EPMC10821870 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Kv3.4 regulates cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition in A549 cells.

Sim Hun Ju HJ Kim Mi Ri MR Song Min Seok MS Lee So Yeong SY

Scientific reports 20240128 1

Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. This process induces cell migration and invasion, which are closely related to cancer metastasis and malignancy. EMT consists of various intermediate states that express both epithelial and mesenchymal traits, called partial EMT. Recently, several studies have focused on the roles of voltage-gated potassium (Kv) channels associated with EMT in cancer cell migration and invasion. ...[more]

PMID: 38280903

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Project description:BackgroundColorectal cancer (CRC) is an aggressive tumor of the gastrointestinal tract, which is a major public health concern worldwide. Despite numerous studies, the precise mechanism of metastasis behind its progression remains elusive. As a member of the containing olfactomedin domains protein family, olfactomedin 2 (OLFM2) may play a role in tumor metastasis. It is highly expressed in colorectal cancer, and its role in the metastasis of CRC is still unclear. As such, this study seeks to explore the function of OLFM2 on CRC metastasis and its potential mechanisms.MethodsReal-time fluorescence quantitative PCR and western blotting were used to study the expression of OLFM2 in human CRC and adjacent normal tissues. Knockdown and overexpression OLFM2 cell lines were constructed using siRNA and overexpression plasmids to explore the role of OLFM2 in the migration and invasion of CRC through transwell, and wound healing experiments. Finally, the expression of epithelial-mesenchymal transition (EMT) -related proteins and TGF-β/Smad signaling pathway-related proteins was investigated using western blotting.ResultsIn this study, we observed an elevation of OLFM2 expression levels in CRC tissues. To investigate the function of OLFM2, we overexpressed and knocked down OLFM2. We discovered that OLFM2 knockdown inhibited migration and invasion of colon cancer cells. Furthermore, E-cadherin expression increased while N-cadherin and Vimentin expression were opposite. It is no surprise that overexpressing OLFM2 had the opposite effects. We also identified that OLFM2 knockdown resulted in reduced TGF-βR1 and downstream molecules p-Smad2 and p-Smad3, which are related to the TGF-β / Smad pathway. In contrast, overexpressing OLFM2 significantly boosted their expression levels.ConclusionThe protein OLFM2 has been identified as a crucial determinant in the progression of CRC. Its mechanism of action involves the facilitation of EMT through the TGF-β/Smad signaling pathway. Given its pivotal role in CRC, OLFM2 has emerged as a promising diagnostic and therapeutic target for the disease. These results indicate the potential of OLFM2 as a valuable biomarker for CRC diagnosis and treatment and highlight the need for further research exploring its clinical significance.

Project description:BackgroundHuman gastric cancer is a serious disease with high mortality rate all over the world. The one of difficulties in effective therapy of gastric cancer is metastasis. It has been reported that lncRNAs and miRNAs are involved in cancer metastasis. So, exploration of new molecular mechanism underlying gastric cancer metastasis involving in network of lncRNAs/miRNAs/effector proteins is important and meaningful for guiding the treatment of gastric cancer.MethodsMTT assay, flow cytometric analysis and colony formation assay were performed to evaluate AGS or MKN-45 cell proliferation, cycle distribution and colony formation, and RT-qPCR was used to examine the expressive abundances of EDIL3, XIST and miR-137. EDIL3 and epithelial-mesenchymal transition (EMT) related proteins were detected by western blot and migration and invasion were measured by transwell analysis. Meanwhile, Dual-luciferase reporter gene assay was used to confirm XIST binding to miR-137, and miR-137 binding to EDIL3. AGS cells were used to establish the xenograft tumor model to verify the role of EDIL3 in tumorigenesis in nude mice.ResultsExpression levels of EDIL3 was increased in gastric cancer tissues and cell lines. Downregulation of EDIL3 or XIST and overexpression of miR-137 inhibited proliferation, migration, invasion and EMT in AGS and MKN-45 cells. XIST could specifically bind to miR-137, and EDIL3 was a target gene of miR-137. Moreover, TGF-β1 stimulated XIST expression, inhibited miR-137 expression and induced migration, invasion and EMT. We also found that overexpression of EDIL3 elevated levels of TGF-β1 and induced migration, invasion and EMT, which were reversed by TGF-β1 inhibition. EDIL3 knockdown suppressed migration, invasion and EMT, which were reversed by XIST. Overexpression of miR-137 inhibited proliferation, migration, invasion and EMT, which were reversed by EDIL3 overexpression.ConclusionsEDIL3 regulates gastric cancer cell migration, invasion and EMT, which is involved in the regulation of TGF-β1/XIST/miR-137 feedback loop, and EDIL3 knockdown inhibits tumor growth in nude mice. These findings indicate that the EDIL3 mediated molecular feedback loop may be developed as drug targets for the gastric carcinoma treatment.

Dataset Information

Kv3.4 regulates cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition in A549 cells.

Publications

Kv3.4 regulates cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition in A549 cells.

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