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We began analyzing https://www.spandidos-publications.com/10.3892/or.2021.7924, but it redirected us to https://www.spandidos-publications.com/10.3892/or.2021.7924. The analysis below is for the second page.

Title[redir]:
Catechol enhances chemo‑ and radio‑sensitivity by targeting AMPK/Hippo signaling in pancreatic cancer cells
Description:
Overcoming chemo‑ and radio‑resistance is a major challenge in pancreatic cancer treatment. Therefore, there is an urgent need to discover novel therapeutic approaches to avoid chemo‑ and radio‑resistance in pancreatic cancer. Catechol is a phytochemical found in some fruits and vegetables. A few studies have reported on the potential anticancer effects of pure catechol. The present study aimed to explore the chemo‑ and radio‑sensitizing effects of catechol in Panc‑1 human pancreatic cancer cells. The effects of catechol on Panc‑1 cell proliferation, clonogenic survival, invasion, and migration were assessed using MTT, cell migration, and Transwell invasion assays. The chemo‑ and radio‑sensitizing effects of catechol on Panc‑1 cells were evaluated via MTT assay and flow cytometry. Western blotting was conducted to analyze the expression of proteins involved in several mechanisms induced by catechol in Panc‑1 cells, including growth inhibition, apoptosis, suppression of epithelial‑mesenchymal transition (EMT), and chemo‑ and radio‑sensitizing activities. The results indicated that catechol inhibited proliferation, promoted apoptosis, and suppressed cell migration, invasion, and EMT in Panc‑1 cells in a dose‑dependent manner. Catechol treatment also induced the phosphorylation of AMP‑activated protein kinase (AMPK) with a concomitant reduction in the expression of Hippo signaling pathway components, including Yes‑associated protein, cysteine‑rich angiogenic inducer 61, and connective tissue growth factor. In addition, catechol enhanced the chemosensitivity of Panc‑1 cells to gemcitabine, a commonly used chemotherapy in pancreatic cancer treatment. A combination of catechol and radiation enhanced apoptosis and increased the expression of two radiation‑induced DNA damage markers, p‑ATM and p‑Chk2. Collectively, the present results demonstrated that catechol, a naturally occurring compound, could suppress the proliferation of pancreatic cancer cells, reduce the expression of EMT‑related proteins, and enhance the chemo‑ and radio‑sensitivity of Panc‑1 cells by targeting AMPK/Hippo signaling.

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Keywords {🔍}

catechol, cells, cancer, panc, pancreatic, cell, article, gemcitabine, view, google, scholar, pubmedncbi, treatment, effects, assay, protein, fig, signaling, expression, revealed, yap, product, analysis, apoptosis, pathway, radiation, results, control, reported, invasion, western, efficacy, levels, present, study, migration, kinase, parp, experiments, cycle, chemo, proteins, emt, ampk, hippo, cyr, blot, radiosensitivity, kim, major,

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gov/services-resources/software/nists-integrated-colony-enumerator-nice erks/c-myc signaling pathway bio-health materials core-facility 1021-335x online issn p-amp-activated protein kinase professor jae-hoon kim induces c-myc degradation plant-derived secondary metabolites radiation-induced dna-damage markers amp‑activated protein kinase amp-activated protein kinase greatest anti-proliferative effect strongest anti-proliferative effect horse anti-mouse immunoglobin advanced-stage pancreatic cancer rhoa/yap signaling axis ampk/hippo signaling pathway atm serine/threonine kinase targeting ampk/hippo signaling synergistic anti-proliferative effects stat3/il-6 survival pathway plant-derived herbal drugs radiation-induced dna damage home submit manuscript endoplasmic reticulum stress chk2-mediated regulation small-cell lung cancer ediriweera mk clinical oncology experimental increased p-ampk levels colony formation assay herbal medicine major clinical issues /hippo signaling pathway hippo signaling pathway cell cycle arrest targets hippo signaling oncology molecular catechol/radiation combined therapy cell signaling technology editor general information camphor induces proliferative dna damage induced nat cell biol promote gemcitabine-induced apoptosis protease-activated receptors moon epithelial‑mesenchymal transition p-checkpoint kinase 2 epithelial-mesenchymal transition

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