(S)-(-)-N-[2-(3-Hydroxy-2-oxo-2,3-dihydro-1H-indol-3-yl)-ethyl]-acetamide inhibits colon cancer growth via the STAT1 pathway

Abstract (S)-(-)-N-[2-(3-Hydroxy-2-oxo-2,3-dihydro-1H-indol-3-yl)-ethyl]-acetamide (EA), a new compound isolated from the plant Selaginella pulvinata, has been identified to possess anti-proliferative effects against SK-mel-110 cells in vitro via upregulating the expression of inhibitor of growth family member 4. The present study aimed to investigate whether EA could exert antitumor effects against colon cancer. The results revealed that EA exerted anti-proliferative effects against a broad spectrum of different types of tumor and could induce apoptosis of colon cancer cells via the signal transducer and activator of transcription 1 pathway. It was demonstrated that treating tumor-bearing mice with EA significantly inhibited colon tumor growth in a xenograft tumor model and syngeneic tumor model. Furthermore, EA treatment reshaped the tumor microenvironment by decreasing myeloid-derived suppressor cell accumulation and increasing the tumor infiltrating lymphocytes. The results from the present study suggest that EA could be developed as a potential antitumor drug against colon cancer.

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Bibliographic Details
Main Authors: LI,Kang, YUAN,Dawei, CHEN,Wei, MA,Rulan, XIAN,Yinsheng
Format: Digital revista
Language:English
Published: Sociedade Brasileira de Ciência e Tecnologia de Alimentos 2022
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100700
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Summary:Abstract (S)-(-)-N-[2-(3-Hydroxy-2-oxo-2,3-dihydro-1H-indol-3-yl)-ethyl]-acetamide (EA), a new compound isolated from the plant Selaginella pulvinata, has been identified to possess anti-proliferative effects against SK-mel-110 cells in vitro via upregulating the expression of inhibitor of growth family member 4. The present study aimed to investigate whether EA could exert antitumor effects against colon cancer. The results revealed that EA exerted anti-proliferative effects against a broad spectrum of different types of tumor and could induce apoptosis of colon cancer cells via the signal transducer and activator of transcription 1 pathway. It was demonstrated that treating tumor-bearing mice with EA significantly inhibited colon tumor growth in a xenograft tumor model and syngeneic tumor model. Furthermore, EA treatment reshaped the tumor microenvironment by decreasing myeloid-derived suppressor cell accumulation and increasing the tumor infiltrating lymphocytes. The results from the present study suggest that EA could be developed as a potential antitumor drug against colon cancer.