Degalactotigonin, a Steroidal Glycoside from Solanum nigrum, Induces Apoptosis and Cell Cycle Arrest via Inhibiting the EGFR Signaling Pathways in Pancreatic Cancer Cells

Author:

Tuan Anh Hoang Le1,Tran Phuong Thao2ORCID,Thao Do Thi3,Trang Duong Thu4,Dang Nguyen Hai4ORCID,Van Cuong Pham4,Kiem Phan Van4,Minh Chau Van4,Lee Jeong-Hyung2ORCID

Affiliation:

1. Mientrung Institute for Scientific Research, Vietnam Academy of Science and Technology (VAST), 321 Huynh Thuc Khang, Hue city, Thua Thien Hue 531600, Vietnam

2. Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, Gangwon-Do 200-701, Republic of Korea

3. Institute of Biotechnology, VAST, 18 Hoang Quoc Viet, Cau Giay, Hanoi, Vietnam

4. Advanced Center for Bio-Organic Chemistry, Institute of Marine Biochemistry, VAST, 18 Hoang Quoc Viet, Cau Giay, Hanoi, Vietnam

Abstract

Degalactotigonin (1) and three other steroidal compounds solasodine (2), O-acetyl solasodine (3), and soladulcoside A (4) were isolated from the methanolic extract of Solanum nigrum, and their chemical structures were elucidated by spectroscopic analyses. The isolated compounds were evaluated for cytotoxic activity against human pancreatic cancer cell lines (PANC1 and MIA-PaCa2) and lung cancer cell lines (A549, NCI-H1975, and NCI-H1299). Only degalactotigonin (1) showed potent cytotoxicity against these cancer cell lines. Compound 1 induced apoptosis in PANC1 and A549 cells. Further study on its mechanism of action in PANC1 cells demonstrated that 1 significantly inhibited EGF-induced proliferation and migration in a concentration-dependent manner. Treatment of PANC1 cells with degalactotigonin induced cell cycle arrest at G0/G1 phase. Compound 1 induced downregulation of cyclin D1 and upregulation of p21 in a time- and concentration-dependent manner and inhibited EGF-induced phosphorylation of EGFR, as well as activation of EGFR downstream signaling molecules such as Akt and ERK.

Funder

National Foundation for Science and Technology Development

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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