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Epithelial-mesenchymal transition induced by MyoD inhibits growth of high metastatic colorectal cancer.
Medical Hypotheses 2019 September
OBJECTIVES: The study aimed to investigate the tumor-suppressing factor myogenicity differentiation factor (MyoD) against high metastatic colorectal cancer through its powerful transformation by which the tumor cells were converted into muscle cells or other cells to inhibit the malignant proliferation of tumor cells.
METHODS: The roles of MyoD in colon cancer proliferation, invasion and migration were analyzed by CCK-8 assay and Transwell, and EMT by real-time PCR and Western blot. The secretion of TGFβ1 was assayed by ELISA and activation of p-Smad2/3 were assayed by western blot. The effects of MyoD on intestinal cancer growth and EMT in vivo were also analyzed.
RESULTS: We found MyoD inhibited the proliferation, invasion and migration of colon cancer cell. Moreover, MyoD inhibited the expression of E-cadherin and promoted the expression of vimentin and α-SMA. The secretion of TGFβ1 increased and p-Smad2/3 was activated after MyoD expression. MyoD also inhibits intestinal cancer growth and promoted EMT in vivo.
CONCLUSION: Our findings indicate that MyoD inhibited cancer progression and metastasis by promoting EMT through TGF-β1/Smad2/3 activation, which provide new support for MyoD maybe as a novel anti-cancer method for the treatment of colon cancer in the future.
METHODS: The roles of MyoD in colon cancer proliferation, invasion and migration were analyzed by CCK-8 assay and Transwell, and EMT by real-time PCR and Western blot. The secretion of TGFβ1 was assayed by ELISA and activation of p-Smad2/3 were assayed by western blot. The effects of MyoD on intestinal cancer growth and EMT in vivo were also analyzed.
RESULTS: We found MyoD inhibited the proliferation, invasion and migration of colon cancer cell. Moreover, MyoD inhibited the expression of E-cadherin and promoted the expression of vimentin and α-SMA. The secretion of TGFβ1 increased and p-Smad2/3 was activated after MyoD expression. MyoD also inhibits intestinal cancer growth and promoted EMT in vivo.
CONCLUSION: Our findings indicate that MyoD inhibited cancer progression and metastasis by promoting EMT through TGF-β1/Smad2/3 activation, which provide new support for MyoD maybe as a novel anti-cancer method for the treatment of colon cancer in the future.
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