Levistolide A Induces Apoptosis via ROS-Mediated ER Stress Pathway in Colon Cancer Cells

Yang, Yingjuan; Zhang, Yanhua; Wang, Lan; Lee, Shaochin

doi:10.1159/000478647

Cited by 65 publications

(44 citation statements)

References 33 publications

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“…Increasing intracellular ROS level can induce ER stress and mitochondrial dysfunction, leading to apoptotic cell death in various intestinal cells such as HCT-8, IEC-6 cells and Caco-2 cells. [38,39] High lelvel of CHOP, an ER stress response-related protein, was related to a decrease in antiapoptotic Bcl-2 protein and an increase in a pro-apoptotic Bax protein. [14,16] Rising of Bax/Bcl-2 expression ratio causes the loss of mitochondria membrane permeability (MMP) and disrupts mitochondria function.…”

Section: Discussionmentioning

confidence: 99%

Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity

Boonyong

Vardhanabhuti

Jianmongkol

2020

Journal of Pharmacy and Pharmacology

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Objectives Indomethacin (INDO) and diclofenac (DIC) can induce intestinal cell death through induction of oxidative stress‐mediated ER stress and mitochondrial dysfunction. This study investigated the cytoprotective potential of 11 polyphenols, namely caffeic acid (CAF), curcumin (CUR), epigallocatechin gallate (EGCG), gallic acid (GAL), hypophyllanthin (HYPO), naringenin (NAR), phyllanthin (PHY), piperine (PIP), quercetin (QUE), rutin (RUT) and silymarin (SLY) against these two NSAIDs in Caco‐2 cells. Methods Reactive oxygen species (ROS) production was determined with fluorescence spectroscopy using specific probes (DHE, DCFH‐DA, HPF). Cell viability and mitochondrial function were assessed by MTT and TMRE assays. The mRNA levels of Bax, Bcl‐2 and CHOP proteins were determined by quantitative real‐time polymerase chain reaction technique. Key findings All test polyphenols reduced NSAIDs‐mediated ROS production. Only EGCG, QUE and RUT protected INDO‐/DIC‐induced cell death. These three polyphenols suppressed Bax/Bcl‐2 mRNA ratio, CHOP up‐regulation and MMP disruption in NSAIDs‐treated cells. CAF and NAR prevented cytotoxicity from INDO, but not DIC. The cytoprotective effect of NAR, but not CAF, involved alteration of Bax/Bcl‐2 mRNA ratio or MMP disruption, but not CHOP transcription. Conclusion The cytoprotective activity of polyphenols against NSAIDs‐induced toxicity stemmed from either suppression of CHOP‐related ER and mitochondria stresses or other CHOP‐independent pathways, but not from the intrinsic ROS scavenging capacity.

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Section: Discussionmentioning

confidence: 99%

Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity

Boonyong

Vardhanabhuti

Jianmongkol

2020

Journal of Pharmacy and Pharmacology

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“…Reactive oxygen species (ROS) are by-products of oxygen metabolism that occur under cellular oxidative stress conditions and play a critical role in the maintenance of homeostasis [37]. Targeting ROS is an important therapeutic strategy for cancer, as exemplified by cancer drugs [38].…”

Section: Discussionmentioning

confidence: 99%

Protodioscin Induces Apoptosis Through ROS-Mediated Endoplasmic Reticulum Stress via the JNK/p38 Activation Pathways in Human Cervical Cancer Cells

Lin

Lee

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Protodioscin (PD) is a steroidal saponin with anti-cancer effects on a number of cancer cells, but the anti-tumor effects and mechanism of action of PD on human cervical cancer cells is unclear. Methods: We determined cell viability using the MTT assay. Cell death, mitochondrial membrane potential (MMP), intracellular reactive oxygen species (ROS) generation, and endoplasmic reticulum (ER) stress were measured on a flow cytometry. Caspase activation, ER stress, and MMP-dependent apoptosis proteins in cervical cancer cells in response to PD were determined by Western blot analysis. The ability of ATF4 binding to ChIP promoter was measured using the ChIP assay. Results: We demonstrated that PD inhibits cell viability, causes a loss of mitochondrial function, and induces apoptosis, as evidenced by up-regulation of caspase-8, -3, -9, -PARP, and Bax activation, and down-regulation of Bcl-2 expression. PD was shown to induce ROS and the ER stress pathway, including GRP78, p-eIF-2α, ATF4, and CHOP. Pre-treatment with NAC, a ROS production inhibitor, significantly reduced ER stress and apoptosis-related proteins induced by PD. Transfection of GRP78/CHOP-siRNA effectively inhibited PD-induced ER stress-dependent apoptosis. Moreover, treatment with PD significantly increased p38 and JNK activation. Co-administration of a JNK inhibitor (SP600125) or p38 inhibitor (SB203580) abolished cell death and ER stress effects during PD treatment. In addition, PD induced the expression of nuclear ATF4 and CHOP, as well as the binding ability of ATF4 to the CHOP promoter. Conclusion: Our results suggest that PD is a promising therapeutic agent for the treatment of human cervical cancer.

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“…Various studies have shown that some natural compounds have an anti‐cancer effect in colon cancer cells. Levistolide A induced apoptosis via the generation of reactive oxygen species and curcumin induced apoptosis via cell cycle arrest in colon cancer cells . Natural compounds have also been used since ancient times for the treatment of various diseases.…”

Section: Introductionmentioning

confidence: 99%

Esculetin induces cell cycle arrest and apoptosis in human colon cancer LoVo cells

Choi

Lee

Park

et al. 2019

Environmental Toxicology

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We investigated the anti‐cancer effects of ESC in human colon cancer LoVo cells. Cell counting assay results showed that ESC inhibited the proliferation of LoVo cells. Cell cycle arrest results showed that cell cycle was arrested during the G0/G1 phase in the ESC‐treated LoVo cells. Western blot results showed that the cell cycle inhibitory proteins p53, p27, and p21 were increased, and cyclin D1, the cell cycle progressive protein, was decreased. Sp1 is a transcription factor regulating cell proliferation, was decreased in the ESC‐treated LoVo cells. Annexin V/propidium iodide staining results showed that ESC induces apoptosis in LoVo cells. Western blot results showed that Bax, cleaved caspase ‐3, ‐7, ‐9, and poly(ADP‐ribose) polymerase, which are proapoptotic proteins, were increased and the antiapoptotic protein Bcl‐2 was decreased. Taken together, ESC induced apoptosis and has an anti‐cancer effect in LoVo cells.

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Levistolide A Induces Apoptosis via ROS-Mediated ER Stress Pathway in Colon Cancer Cells

Cited by 65 publications

References 33 publications

Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity

Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity

Protodioscin Induces Apoptosis Through ROS-Mediated Endoplasmic Reticulum Stress via the JNK/p38 Activation Pathways in Human Cervical Cancer Cells

Esculetin induces cell cycle arrest and apoptosis in human colon cancer LoVo cells

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