ArticleExperimental and therapeutic medicine2020
Anti-tumor peptide SA12 inhibits metastasis of MDA-MB-231 and MCF-7 breast cancer cells via increasing expression of the tumor metastasis suppressor genes, CDH1, nm23-H1 and BRMS1.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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6 authors at 1 institution in 1 country.
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Abstract
In recent years, there has been progress in the treatment of breast cancer; however, the prognosis is still poor due to recurrence and metastasis following conventional treatment. The anti-tumor peptide SA12 has been demonstrated to inhibit proliferation and arrest the cell cycle in MDA-MB-231 and MCF-7 breast cancer cells. In the present study, whether SA12 was able to inhibit the metastasis of breast cancer cells was investigated. Wound healing and Transwell assays were used to investigate the inhibition of SA12 on cell migration while, reverse transcription-quantitative PCR and western blot assays were used to identify the mechanism of action behind the effects of SA12 on cell migration. Results from the wound healing and Transwell assays revealed that SA12 significantly inhibited the migration of MDA-MB-231 and MCF-7 breast cancer cells following treatment with 100 µM SA12. Compared with that in the controls, the mRNA expression levels of cadherin 1 (CDH1), non-metastasis 23-H1 (nm23-H1) and breast cancer metastasis suppressor 1 (BRMS1) were increased in MDA-MB-231 and MCF-7 cells following treatment with 100 µM SA12. Furthermore, the protein expression levels of E-cadherin, NM23A and BRMS1 were also increased in MDA-MB-231 cells and MCF-7 cells following treatment with 100 µM SA12. In conclusion, SA12 inhibited the migration of MDA-MB-231 and MCF-7 breast cancer cells and enhanced the expression of the tumor metastasis suppressor genes, CDH1, nm23-H1 and BRMS1, which may be responsible for the SA12-induced inhibition of breast cancer cell metastasis.
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