The anti-cancer activity of resveratrol in human esophageal squamous cell carcinoma (ESCC) was investigated focusing on the role of autophagy and its effects on apoptotic cell death. We demonstrated that resveratrol inhibits ESCC cell growth in a dose-dependent manner by inducing cell cycle arrest at the sub-G1 phase and resulting in subsequent apoptosis. Mechanistically, resveratrol-induced autophagy in the ESCC cells is AMPK/mTOR pathway independent. Since both pharmacological and genetic inhibition of autophagy enhanced the resveratrol-induced cytotoxicity to the ESCC cells, this provided a novel strategy in potentiating the anti-cancer effects of resveratrol and other chemotherapeutic reagents in ESCC cancer treatment.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.canlet.2013.03.023 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Deep learning identification of novel autophagic protein-protein interactions and experimental validation of Beclin 2-Ubiquilin 1 axis in triple-negative breast cancer.
Oncol Res
December 2024
Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Background: Triple-negative breast cancer (TNBC), characterized by its lack of traditional hormone receptors and HER2, presents a significant challenge in oncology due to its poor response to conventional therapies. Autophagy is an important process for maintaining cellular homeostasis, and there are currently autophagy biomarkers that play an effective role in the clinical treatment of tumors. In contrast to targeting protein activity, intervention with protein-protein interaction (PPI) can avoid unrelated crosstalk and regulate the autophagy process with minimal interference pathways.
View Article and Find Full Text PDFLong noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy.
Oncol Res
December 2024
Department of Respiratory and Critical Care Medicine, Nanping First Hospital Affiliated to Fujian Medical University, Nanping, 353006, China.
Background: Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear.
Methods: LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth.
Icariside II relieves radiation enteritis by regulating PINK/Parkin-mediated mitophagy.
Int Immunopharmacol
December 2024
Changchun University of Chinese Medicine, Changchun, China; Department of Urology, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, China. Electronic address:
Radiation enteritis (RE) is one of the major side effects of radiotherapy. So far, there are no effective drugs for preventing the disease process. Icariside II (ICS II) is a highly efficient monomer compound extracted and purified from the classic Chinese medicinal herb Epimedium.
View Article and Find Full Text PDFResolvin D1 combined with exercise rehabilitation alleviates neurological injury in mice with intracranial hemorrhage via the BDNF/TrkB/PI3K/AKT pathway.
Sci Rep
December 2024
School of Basic Medicine, Dali University, Dali, 671003, Yunnan, China.
Resolvin D1 (RvD1) is an endogenous anti-inflammatory mediator that modulates the inflammatory response and promotes inflammation resolution. RvD1 has demonstrated neuroprotective effects in various central nervous system contexts; however, its role in the pathophysiological processes of intracerebral hemorrhage (ICH) and the potential protective mechanisms when combined with exercise rehabilitation remain unclear. A mouse model of ICH was established using collagenase, and treatment with RvD1 combined with three weeks of exercise rehabilitation significantly improved neurological deficits, muscle strength, learning, and memory in ICH mice while reducing anxiety-like behavior.
View Article and Find Full Text PDFHypoxia-induced TPC2 transcription and glycosylation aggravates pulmonary arterial hypertension by blocking autophagy flux.
Sci Rep
December 2024
Department of Respiratory Medicine, Hunan Provincial People's Hospital (The First-Affiliated Hospital of Hunan Normal University), No. 61 Jiefang Xi Road, Changsha, Hunan, 410219, China.
Pulmonary arterial hypertension (PAH) is a serious medical condition that causes a failure in the right heart. Two-pore channel 2 (TPC2) is upregulated in PAH, but its roles in PAH remain largely unknown. Our investigation aims at the mechanisms by which TPC2 regulates PAH development.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!