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Med Hypotheses. 2019 Sep;130:109285. doi: 10.1016/j.mehy.2019.109285. Epub 2019 Jun 24.

Epithelial-mesenchymal transition induced by MyoD inhibits growth of high metastatic colorectal cancer.

Author information

1
Department of General Surgery, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, Hubei, China.
2
Digestive Department, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, Hubei, China.
3
Department Surgery, Hubei Province Nanzhang County Hospital of Traditional Chinese Medicine, Xiangyang 441021, Hubei, China.
4
Pathology Department, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, Hubei, China. Electronic address: jingyangsdu@126.com.

Abstract

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.

KEYWORDS:

Colon cancer; E-cadherin; Epithelial-mesenchymal transition; High metastatic; Myogenicity differentiation factor

PMID:
31383323
DOI:
10.1016/j.mehy.2019.109285
[Indexed for MEDLINE]

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