Suppression of Migration and Invasion by 4-Carbomethoxyl-10-Epigyrosanoldie E from the Cultured Soft Coral Sinularia sandensis through the MAPKs Pathway on Oral Cancer Cells

Sep 21, 2026

Uploaded by Patrick

Oral cancer fatalities are driven largely by metastasis, making inhibition of tumor cell migration and invasion a key therapeutic goal. This study evaluates 4-carbomethoxyl-10-epigyrosanoldie E, a cultured soft-coral compound from Sinularia sandensis, for its effects on Cal-27 and Ca9-22 oral cancer cells. Dose-dependent results show reduced MMP-2/MMP-9 and uPA, increased TIMP-1/TIMP-2, and decreased ERK, p38, and JNK phosphorylation, alongside lowered expression of adhesion and signaling proteins, implicating MAPKs pathway suppression.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages11

Reading Time28 min

AccessFree to download

Introduction

Metastasis and the need for targeted therapies

MAPK signaling in cancer progression

Marine soft corals as sources of bioactive compounds

Methods

Cell migration and invasion assessment (Boyden chamber)

Molecular mechanism analysis (Western blot)

Results

Changes in MMPs, uPA, and TIMPs

MAPKs pathway phosphorylation and downstream proteins

Hindawi Advances in Pharmacological and Pharmaceutical Sciences Volume 2024, Article ID 6695837, 11 pages [https://doi.org/10.1155/2024/6695837](https://doi.org/10.1155/2024/6695837) Research Article Suppression of Migration and Invasion by 4-Carbomethoxyl-10-Epigyrosanoldie E from the Cultured Soft Coral Sinularia sandensis through the MAPKs Pathway on Oral Cancer Cells Rou-Yi Fang, 1,2 Yueh-Wen Liu,3 Yih-Gang Goan,4 Jen-Jie Lin,5 Jui-Hsin Su,6 Wen-Tung Wu ,7 and Yu-Jen Wu 5 1 Department of Pharmacy, Kaohsiung Veterans General Hospital, Pingtung Branch, Kaohsiung, Taiwan 2 Department of Nursing, Meiho University, Pingtung, Taiwan 3 Department of Cosmetics and Fashion Styling, Cheng Shiu University, Kaohsiung, Taiwan 4 Division of Toracic Surgery Department of Surgery, Pingtung Veterans General Hospital, Pingtung, Taiwan 5 Yu Jun Biotechnology Co., Ltd., Kaohsiung, Taiwan 6 National Museum of Marine Biology and Aquarium, Pingtung 94450, Taiwan 7 Department of Food Science and Nutrition, Meiho University, Pingtung 91202, Taiwan Correspondence should be addressed to Wen-Tung Wu; [gerrywu8769@yahoo.com.tw and Yu-Jen Wu](gerrywu8769@yahoo.com.tw and Yu-Jen Wu); wyr924@ms24.hinet.net Received 8 August 2023; Revised 27 December 2023; Accepted 20 January 2024; Published 12 February 2024 Academic Editor: Norsharina Ismail Copyright © 2024 Rou-Yi Fang et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Te primary reason for cancer-related fatalities is metastasis. Te compound 4-carbomethoxyl-10-epigyrosanoldie E, derived from the Sinularia sandensis soft coral species grown in cultures, exhibits properties that counteract infammation. Moreover, it has been observed to trigger both apoptosis and autophagy within cancerous cells. Tis research focuses on examining the inhibitory impact of 4-carbomethoxyl-10-epigyrosanoldie E on the migration and invasion processes in Cal-27 and Ca9-22 oral cancer cell lines. To assess how this compound afects cell migration and invasion, the Boyden chamber assay was employed. Furthermore, Western blot analysis was utilized to explore the underlying molecular mechanisms. In a dose-dependent manner, 4-carbomethoxyl-10-epigyrosanoldie E notably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9, along with urokinase-type plasminogen activator (uPA), in both Cal-27 and Ca9-22 cell lines. Conversely, it elevated the concentrations oftissue inhibitors of metalloproteinases-1 (TIMP-1) and TIMP-2. In addition, the treatment with this compound led to the inhibition of phosphorylation in extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). It also curtailed the expression of several key proteins including focal adhesion kinase (FAK), protein kinase C (PKC), growth factor receptor-bound protein 2 (GRB2), Rac, Ras, Rho A, mitogen-activated protein kinasekinase kinase 3 (MEKK3), and mitogen-activated protein kinase kinase 7 (MKK7). Furthermore, the expression levels of IQ-domain GTPase-activating protein 1 (IQGAP1) and zonula occludens-1 (ZO-1) were signifcantly reduced by the compound. Te ability of 4-carbomethoxyl-10-epigyrosanoldie E to inhibit the migration and invasion of Cal-27 and Ca9-22 oral cancer cells was observed to be dose dependent. Tis inhibitory efect is primarily attributed to the suppression of MMP-2 and MMP-9 expression, as well as the downregulation of the mitogen-activated protein kinase (MAPK) signaling pathway. 1. Introduction Oral cancer most commonly develops from the squamous cells lining the mouth, with oral squamous cell carcinoma (OSCC) accounting for approximately 90% of these cases [1] . Major risk factors contributing to the development of oral cancer are the consumption of betel nuts, tobacco use, and alcohol intake. Tese factors are

FAQs

How does 4-carbomethoxyl-10-epigyrosanoldie E affect migration and invasion in oral cancer cells?

The compound inhibits migration and invasion in Cal-27 and Ca9-22 cells in a dose-dependent manner.

Which molecular markers are altered by the treatment?

Treatment decreases MMP-2, MMP-9, and uPA, while increasing TIMP-1 and TIMP-2.

What signaling pathway is implicated in the observed anti-metastatic effects?

Inhibition of MAPKs pathway signaling is supported by reduced phosphorylation of ERK, p38, and JNK and decreased expression of multiple downstream proteins.

Sep 21, 2026

Uploaded by Patrick