P38 MAP kinase functions as a switch in MS-275-induced reactive oxygen species-dependent autophagy and apoptosis in Human colon Cancer cells

Yao, Zhan; Gong, Kan; Chen, Chao; Wang, Haiqing; Li, Wenhua

doi:10.1016/j.freeradbiomed.2012.05.018

Cited by 67 publications

(46 citation statements)

References 51 publications

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“…Imbalance of cellular ROS could lead to cell death in different circumstances (Park et al, 2012;Zhan et al, 2012). In our present study, the generation of ROS induced by TG was detected using the specific fluorescence probe DCFH-DA.…”

Section: Ros Mediates Apoptosis and Autophagy Induced By Tg In Hepg2 mentioning

confidence: 78%

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway

Wang

Tang

et al. 2016

Environmental Toxicology and Pharmacology

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Section: Ros Mediates Apoptosis and Autophagy Induced By Tg In Hepg2 mentioning

confidence: 78%

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway

Wang

Tang

et al. 2016

Environmental Toxicology and Pharmacology

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“…[10][11][12] However, in contrast to hematologic [39][40][41] or some selected other gastrointestinal tract tumors, [42][43][44] , the potential of epigenetic-based therapy has not yet been widely addressed in esophageal cancer. So far, treatment advances of the highly aggressive esophageal cancers are by surgery and radiochemotherapy.…”

Section: Discussionmentioning

confidence: 99%

“…52 Specifically, so far only few other groups focusing on solid cancers have addressed the effects of HDACi on paired non-neoplastic and corresponding cancer cell lines, especially not for cells derived from the same epithelial origin. 33,43,53 For instance, Lee at al. 33 compared normal foreskin fibroblast to non-small cell lung cancer and prostate cancer cells-i.e.…”

Section: Discussionmentioning

confidence: 99%

Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine

Ahrens¹,

Timme

Hoeppner³

et al. 2015

Epigenetics

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Esophageal cancers are highly aggressive tumors with poor prognosis despite some recent advances in surgical and radiochemotherapy treatment options. This study addressed the feasibility of drugs targeting epigenetic modifiers in esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) cells. We tested inhibition of histone deacetylases (HDACs) by SAHA, MS-275, and FK228, inhibition of DNA methyltransferases by Azacytidine (AZA) and Decitabine (DAC), and the effect of combination treatment using both types of drugs. The drug targets, HDAC1/2/3 and DNMT1, were expressed in normal esophageal epithelium and tumor cells of ESCC or EAC tissue specimens, as well as in non-neoplastic esophageal epithelial (Het-1A), ESCC (OE21, Kyse-270, Kyse-410), and EAC (OE33, SK-GT-4) cell lines. In vitro, HDAC activity, histone acetylation, and p21 expression were similarly affected in non-neoplastic, ESCC, and EAC cell lines post inhibitor treatment. Combined MS-275/AZA treatment, however, selectively targeted esophageal cancer cell lines by inducing DNA damage, cell viability loss, and apoptosis, and by decreasing cell migration. Non-neoplastic Het-1A cells were protected against HDACi (MS-275)/AZA treatment. RNA transcriptome analyses post MS-275 and/or AZA treatment identified novel regulated candidate genes (up: BCL6, Hes2; down: FAIM, MLKL), which were specifically associated with the treatment responses of esophageal cancer cells. In summary, combined HDACi/AZA treatment is efficient and selective for the targeting of esophageal cancer cells, despite similar target expression of normal and esophageal cancer epithelium, in vitro and in human esophageal carcinomas. The precise mechanisms of action of treatment responses involve novel candidate genes regulated by HDACi/AZA in esophageal cancer cells. Together, targeting of epigenetic modifiers in esophageal cancers may represent a potential future therapeutic approach.

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“…Cetuximab (an antibody for EGFR) generates autophagy and it is currently used to treat KRas mutationnegative, EGFR expressing, metastatic CRC [121] . Moreover, MS275, a synthetic benzamide derivative of HDAC, promoted Atg7 protein expression and induced autophagy to switch to apoptosis through the modulation of p38 in human colon cancer cells [132] . Curcumin is a natural polyphenolic compound that is isolated from the plant Curcuma longa.…”

Section: Autophagy Drugs In Crcmentioning

confidence: 99%

Autophagy in colorectal cancer: An important switch from physiology to pathology

Burada

Nicoli

Ciurea

et al. 2015

WJGO

138

131

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Colorectal cancer (CRC) remains a leading cause of cancer death in both men and women worldwide. Among the factors and mechanisms that are involved in the multifactorial etiology of CRC, autophagy is an important transformational switch that occurs when a cell shifts from normal to malignant. In recent years, multiple hypotheses have been considered regarding the autophagy mechanisms that are involved in cancer. The currently accepted hypothesis is that autophagy has dual and contradictory roles in carcinogenesis, but the precise mechanisms leading to autophagy in cancer are not yet fully defined and seem to be context dependent. Autophagy is a surveillance mechanism used by normal cells that protects them from the transformation to malignancy by removing damaged organelles and aggregated proteins and by reducing reactive oxygen species, mitochondrial abnormalities and DNA damage. However, autophagy also supports tumor formation by promoting access to nutrients that are critical to the metabolism and growth of tumor cells and by inhibiting cellular death and increasing drug resistance. Autophagy studies in CRC have focused on several molecules, mainly microtubule-associated protein 1 light chain 3, beclin 1, and autophagy related 5, with conflicting results. Beneficial effects were observed for some agents that modulate autophagy in CRC either alone or, more often, in combination with other agents. More extensive studies are needed in the future to clarify the roles of Core tip: This review describes the role of autophagy in cancer, focusing on the involvement of autophagy in colorectal cancer (CRC). Initially, we describe the steps and components of autophagy, and we then further highlight the dual role of autophagy in cancer, where it can potentially act as both a promoter and an inhibitor during the transformation from normal to malignant cell. In particular, we emphasize the major autophagy genes involved in CRC pathogenesis along with autophagymodulating agents and their modes of action in the context of CRC therapy. TOPIC HIGHLIGHT

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P38 MAP kinase functions as a switch in MS-275-induced reactive oxygen species-dependent autophagy and apoptosis in Human colon Cancer cells

Cited by 67 publications

References 51 publications

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway

Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine

Autophagy in colorectal cancer: An important switch from physiology to pathology

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