---
title: "EGCG plus thermal cycling reduces NSCLC cell viability via ER stress and Ca2+ dysregulation"
id: "pubmed-42885290"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42885290"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42885290/"
doi: "10.3892/mmr.2026.14043"
published_at: "2026-10-16T12:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# EGCG plus thermal cycling reduces NSCLC cell viability via ER stress and Ca2+ dysregulation
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42885290
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42885290/)
- **DOI:** [10.3892/mmr.2026.14043](https://doi.org/10.3892%2Fmmr.2026.14043)
- **Published At:** 2026-10-16T12:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study assessed combined anticancer effects of **EGCG** and thermal cycling‑stimulation (TCS) on non‑small‑cell lung cancer (**NSCLC**) cell lines. - Investigators tested the combination on A549 and NCI‑H460 tumor lines and compared cytotoxicity with IMR‑90 normal lung fibroblasts, finding selective tumor cell killing with minimal effect on normal cells. - The combination produced a synergistic decrease in cell viability; the source did not report exact dosing regimens or time courses in the abstract. - Authors reported that **EGCG** attenuated TCS‑induced upregulation of heat shock proteins HSP70 and HSP105 while proteasome subunit expression also fell, consistent with disrupted proteostasis. - Data indicated activation of endoplasmic reticulum (ER) stress pathways after combined treatment and implicated inositol 1,4,5‑trisphosphate receptor (IP3R)‑mediated ER Ca2+ release in downstream events. - Pharmacological inhibition experiments, as summarized in the abstract, suggested a bidirectional interplay between ER Ca2+ release and excessive reactive oxygen species (ROS) production that culminated in mitochondrial apoptosis. - The authors concluded the combined therapy reduced the necessary dose of **EGCG** and blunted TCS‑induced heat shock responses; the study is presented as an in vitro proof‑of‑concept. - The abstract does not provide numerical endpoints, statistical values, or detailed experimental parameters such as concentrations, durations, or inhibitor identities; these were not reported in the abstract text.
## Clinical Analysis & Structured Key Points
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Epub 2026 Oct 16. # Epigallocatechin gallate and thermal cycling‑stimulation synergistically promote apoptosis in A549 cells via endoplasmic reticulum stress‑induced calcium ion dysregulation and oxidative stress [Fang-Tzu Hsu](https://pubmed.ncbi.nlm.nih.gov/?term=Hsu+FT&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#full-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C."), [Hsu-Hsiang Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+HH&cauthor_id=42885290)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#full-view-affiliation-2 "Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C."), [Yi Kung](https://pubmed.ncbi.nlm.nih.gov/?term=Kung+Y&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#full-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C."), [Chieh-Jou Lin](https://pubmed.ncbi.nlm.nih.gov/?term=Lin+CJ&cauthor_id=42885290)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#full-view-affiliation-2 "Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C."), [Chih-Yu Chao](https://pubmed.ncbi.nlm.nih.gov/?term=Chao+CY&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#full-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C.") Affiliations Expand ### Affiliations * 1 Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C. * 2 Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C. * PMID: **42885290** * DOI: [ 10.3892/mmr.2026.14043 ](https://doi.org/10.3892/mmr.2026.14043) Item in Clipboard # Epigallocatechin gallate and thermal cycling‑stimulation synergistically promote apoptosis in A549 cells via endoplasmic reticulum stress‑induced calcium ion dysregulation and oxidative stress Fang-Tzu Hsu et al. Mol Med Rep. 2026 Dec. Show details Display options Display options Format Abstract PubMed PMID Mol Med Rep Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Mol+Med+Rep%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Mol+Med+Rep%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42885290/) . 2026 Dec;34(6):332. doi: 10.3892/mmr.2026.14043. Epub 2026 Oct 16. ### Authors [Fang-Tzu Hsu](https://pubmed.ncbi.nlm.nih.gov/?term=Hsu+FT&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#short-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C."), [Hsu-Hsiang Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+HH&cauthor_id=42885290)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#short-view-affiliation-2 "Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C."), [Yi Kung](https://pubmed.ncbi.nlm.nih.gov/?term=Kung+Y&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#short-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C."), [Chieh-Jou Lin](https://pubmed.ncbi.nlm.nih.gov/?term=Lin+CJ&cauthor_id=42885290)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#short-view-affiliation-2 "Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C."), [Chih-Yu Chao](https://pubmed.ncbi.nlm.nih.gov/?term=Chao+CY&cauthor_id=42885290)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885290/#short-view-affiliation-1 "Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C.") ### Affiliations * 1 Department of Physics, Laboratory for Medical Physics and Biomedical Engineering, National Taiwan University, Taipei 106319, Taiwan, R.O.C. * 2 Molecular Imaging Center, National Taiwan University College of Medicine, Taipei 100233, Taiwan, R.O.C. * PMID: **42885290** * DOI: [ 10.3892/mmr.2026.14043 ](https://doi.org/10.3892/mmr.2026.14043) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Non‑small cell lung cancer (NSCLC), as the predominant subtype of lung cancer, presents a considerable clinical challenge due to its high rates of recurrence and the significant adverse effects associated with conventional therapeutic modalities. In response to these challenges, the present study has explored the combined anticancer effects of epigallocatechin gallate (EGCG) together with thermal cycling‑stimulation (TCS). The findings obtained demonstrated that the combination of EGCG and TCS led to a synergistic decrease in the viability of A549 and NCI‑H460 NSCLC cells, whereas IMR‑90 normal lung fibroblasts exhibited minimal cytotoxic effects. Further investigations revealed that EGCG could mitigate the TCS‑induced upregulation of the heat shock proteins (HSPs) HSP70 and HSP105, whereas the expression levels of proteasome subunits were concurrently decreased. These alterations were accompanied by the disruption of proteostasis, and also by the activation of endoplasmic reticulum (ER) stress‑associated pathways. Furthermore, pharmacological inhibition studies suggested a mutual interplay between inositol 1,4,5‑trisphosphate receptor‑mediated ER Ca2+ release and an excessive production of reactive oxygen species, ultimately causing the cells to undergo mitochondrial apoptosis. In summary, the present study has shown that the combined treatment of EGCG and TCS reduces the required dosage of EGCG, while also attenuating TCS‑induced heat shock responses. Consequently, the present study offers a novel and promising _in vitro_ proof‑of‑concept strategy for treating NSCLC. **Keywords:** EGCG; NSCLC; combination treatment; hyperthermia. 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