Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells

Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments....

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Main Authors: Yi-Ting Chen, Tzu-Ting Tseng, Hung-Pei Tsai, Ming-Yii Huang
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/10/5645
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author Yi-Ting Chen
Tzu-Ting Tseng
Hung-Pei Tsai
Ming-Yii Huang
author_facet Yi-Ting Chen
Tzu-Ting Tseng
Hung-Pei Tsai
Ming-Yii Huang
author_sort Yi-Ting Chen
collection DOAJ
description Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC.
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spelling doaj.art-f46f8b7538c14add992679e2b5d7964e2023-11-23T11:26:11ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-05-012310564510.3390/ijms23105645Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer CellsYi-Ting Chen0Tzu-Ting Tseng1Hung-Pei Tsai2Ming-Yii Huang3Department of Pathology, Kaohsiung Medical University Hospital, Kaohsiung 80708, TaiwanDepartment of Pathology, Kaohsiung Medical University Hospital, Kaohsiung 80708, TaiwanDepartment of Surgery, Division of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung 80708, TaiwanDepartment of Radiation Oncology, Kaohsiung Medical University Hospital, Kaohsiung 80708, TaiwanColorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC.https://www.mdpi.com/1422-0067/23/10/5645Arylquin 1colon cancertumor progressionapoptosis
spellingShingle Yi-Ting Chen
Tzu-Ting Tseng
Hung-Pei Tsai
Ming-Yii Huang
Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
International Journal of Molecular Sciences
Arylquin 1
colon cancer
tumor progression
apoptosis
title Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
title_full Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
title_fullStr Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
title_full_unstemmed Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
title_short Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
title_sort arylquin 1 potent par 4 secretagogue inhibits tumor progression and induces apoptosis in colon cancer cells
topic Arylquin 1
colon cancer
tumor progression
apoptosis
url https://www.mdpi.com/1422-0067/23/10/5645
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AT hungpeitsai arylquin1potentpar4secretagogueinhibitstumorprogressionandinducesapoptosisincoloncancercells
AT mingyiihuang arylquin1potentpar4secretagogueinhibitstumorprogressionandinducesapoptosisincoloncancercells