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Main Authors: Chang, Yun-Ching, Lan, Yu-Yan, Lin, Hung-Yu, Liu, Cheng, Chang, Sue-Joan
Format: Artículo científico
Language:en
Published: Journal of oral biosciences 2025
Subjects:
Online Access:https://pubmed.ncbi.nlm.nih.gov/39709169/
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author Chang, Yun-Ching
Lan, Yu-Yan
Lin, Hung-Yu
Liu, Cheng
Chang, Sue-Joan
author_facet Chang, Yun-Ching
Lan, Yu-Yan
Lin, Hung-Yu
Liu, Cheng
Chang, Sue-Joan
Chang, Yun-Ching
Lan, Yu-Yan
Lin, Hung-Yu
Liu, Cheng
Chang, Sue-Joan
collection PubMed - marine biology
contents Low-molecular-weight polyphenol promotes cell sensitivity to cisplatin and alleviates cancer-related muscle atrophy via NF-κB suppression in oral squamous cell carcinoma. Chang, Yun-Ching Lan, Yu-Yan Lin, Hung-Yu Liu, Cheng Chang, Sue-Joan Cisplatin Humans NF-kappa B Muscular Atrophy Mouth Neoplasms Carcinoma, Squamous Cell Cell Line, Tumor Drug Resistance, Neoplasm Antineoplastic Agents Polyphenols Tumor Microenvironment Apoptosis Signal Transduction Cell Survival Interleukin-6 Drug resistance and subsequent adverse effects, such as cancer cachexia, limit the clinical use of cisplatin. Oligonol® (Olg), a low-molecular-weight polyphenol, exhibits NF-κB inhibitory properties. NF-κB activation has been implicated in cisplatin resistance of cancer cells and skeletal muscle wasting. Therefore, we hypothesized that combined cisplatin and Olg could overcome chemoresistance and reduce muscle atrophy. To investigate the efficiency of Olg, oral squamous cell carcinoma (OSCC) cells were used for chemosensitivity, and human skeletal muscle myoblast (HSkMC) was used for muscle atrophy. HSkMCs treated with OSCC cell-derived conditioned medium were used to examine the role of Olg in muscle atrophy mediated by the tumor inflammatory microenvironment. Olg exerted little effect on the viability of OSCC cells by promoting apoptotic cell death. However, it exhibited excellent capability to enhance the sensitivity of OSCC cells to cisplatin and overcome the acquired cisplatin resistance of OSCC. We revealed that NF-κB signaling contributes to cisplatin resistance in OSCC cells, whereas Olg enhances cell sensitivity to cisplatin by NF-κB suppression. Conversely, Olg contributes to a positive protein turnover and alleviates cisplatin-induced muscle atrophy by regulating Akt/mTOR/p70S6K and NF-κB/MuRF1 pathway. Olg represses TNF-α and interleukin 6 driven from OSCC cells and alleviates muscle atrophy mediated by the tumor inflammatory microenvironment. Olg enhanced cisplatin chemosensitivity and reduced its adverse effects on skeletal muscle, suggesting its potential as a chemosensitizing agent for cisplatin. Further animal and clinical studies are required to validate these findings.
format Artículo científico
id pubmed_39709169
institution PubMed
language en
publishDate 2025
publisher Journal of oral biosciences
record_format pubmed
spellingShingle Low-molecular-weight polyphenol promotes cell sensitivity to cisplatin and alleviates cancer-related muscle atrophy via NF-κB suppression in oral squamous cell carcinoma.
Chang, Yun-Ching
Lan, Yu-Yan
Lin, Hung-Yu
Liu, Cheng
Chang, Sue-Joan
Cisplatin
Humans
NF-kappa B
Muscular Atrophy
Mouth Neoplasms
Carcinoma, Squamous Cell
Cell Line, Tumor
Drug Resistance, Neoplasm
Antineoplastic Agents
Polyphenols
Tumor Microenvironment
Apoptosis
Signal Transduction
Cell Survival
Interleukin-6
Low-molecular-weight polyphenol promotes cell sensitivity to cisplatin and alleviates cancer-related muscle atrophy via NF-κB suppression in oral squamous cell carcinoma. Chang, Yun-Ching Lan, Yu-Yan Lin, Hung-Yu Liu, Cheng Chang, Sue-Joan Cisplatin Humans NF-kappa B Muscular Atrophy Mouth Neoplasms Carcinoma, Squamous Cell Cell Line, Tumor Drug Resistance, Neoplasm Antineoplastic Agents Polyphenols Tumor Microenvironment Apoptosis Signal Transduction Cell Survival Interleukin-6 Drug resistance and subsequent adverse effects, such as cancer cachexia, limit the clinical use of cisplatin. Oligonol® (Olg), a low-molecular-weight polyphenol, exhibits NF-κB inhibitory properties. NF-κB activation has been implicated in cisplatin resistance of cancer cells and skeletal muscle wasting. Therefore, we hypothesized that combined cisplatin and Olg could overcome chemoresistance and reduce muscle atrophy. To investigate the efficiency of Olg, oral squamous cell carcinoma (OSCC) cells were used for chemosensitivity, and human skeletal muscle myoblast (HSkMC) was used for muscle atrophy. HSkMCs treated with OSCC cell-derived conditioned medium were used to examine the role of Olg in muscle atrophy mediated by the tumor inflammatory microenvironment. Olg exerted little effect on the viability of OSCC cells by promoting apoptotic cell death. However, it exhibited excellent capability to enhance the sensitivity of OSCC cells to cisplatin and overcome the acquired cisplatin resistance of OSCC. We revealed that NF-κB signaling contributes to cisplatin resistance in OSCC cells, whereas Olg enhances cell sensitivity to cisplatin by NF-κB suppression. Conversely, Olg contributes to a positive protein turnover and alleviates cisplatin-induced muscle atrophy by regulating Akt/mTOR/p70S6K and NF-κB/MuRF1 pathway. Olg represses TNF-α and interleukin 6 driven from OSCC cells and alleviates muscle atrophy mediated by the tumor inflammatory microenvironment. Olg enhanced cisplatin chemosensitivity and reduced its adverse effects on skeletal muscle, suggesting its potential as a chemosensitizing agent for cisplatin. Further animal and clinical studies are required to validate these findings.
title Low-molecular-weight polyphenol promotes cell sensitivity to cisplatin and alleviates cancer-related muscle atrophy via NF-κB suppression in oral squamous cell carcinoma.
topic Cisplatin
Humans
NF-kappa B
Muscular Atrophy
Mouth Neoplasms
Carcinoma, Squamous Cell
Cell Line, Tumor
Drug Resistance, Neoplasm
Antineoplastic Agents
Polyphenols
Tumor Microenvironment
Apoptosis
Signal Transduction
Cell Survival
Interleukin-6
url https://pubmed.ncbi.nlm.nih.gov/39709169/