Capsaicin mediates caspases activation and induces apoptosis through P38 and JNK MAPK pathways in human renal carcinoma

Liu, Tao; Wang, Gang; Tao, Huangheng; Yang, Zhonghua; Wang, Yongzhi; Meng, Zhe; Cao, Rui; Xiao, Yu; Wang, Xinghuan; Zhou, Jiajie

doi:10.1186/s12885-016-2831-y

Cited by 51 publications

(39 citation statements)

References 37 publications

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“…Inhibition of the JNK pathways in cardiomyocytes results in attenuated hypertrophic growth induced by agonist stimulation (28). In addition, previous studies have demonstrated that the activation of JNK is involved in the induction of the inflammatory response and apoptosis (29,30). The present study revealed that DIM inhibited the phosphorylation of JNK in hypoxia-induced H9c2 cells, which indicated that the anti-apoptosis effect of DIM may mediated by blocking JNK pathway.…”

Section: Discussionsupporting

confidence: 62%

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Liang

Qian

Zong

2017

Molecular Medicine Reports

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Autophagy is activated in the ischemic heart and is a process that is essential for survival, differentiation, development and homeostasis. 3,3'‑Diindolylmethane (DIM) is a natural product of the acid‑catalyzed condensation of indole‑3‑carbinol in cruciferous vegetables. Numerous studies have suggested that DIM has various pharmacological effects, including antioxidant, antitumor, anti‑angiogenic and anti‑apoptotic properties. However, the function of DIM on hypoxia‑induced cardiac injury remains to be elucidated. In the present study, H9c2 cells were pretreated with DIM (1, 5 and 10 µM) for 12 h and exposed to hypoxia for 12 h. It was demonstrated that DIM markedly attenuated the increased transcription of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α induced by hypoxia. In addition, the transcription of autophagy associated genes increased in the DIM pretreated group, compared with the hypoxia group. DIM additionally attenuated the increased apoptosis, as determined by terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and regulated the relative protein expression level of B cell lymphoma (Bcl) 2 associated X protein, Bcl‑xL and cleaved caspase 3. Furthermore, the phosphorylation of the 5' AMP‑activated protein kinase a (AMPKa) was activated and the phosphorylation of c‑Jun N‑terminal kinase (JNK) was inhibited. The effect of DIM on hypoxia‑induced apoptosis was abolished following pretreatment with JNK activator (anisomycin, 40 ng/ml). The effect of DIM on autophagy was reversed following pretreatment with AMPKa inhibitor (CpC, 20 µM) following stimulation with hypoxia. The results demonstrated that DIM prevented hypoxia‑induced inflammation and apoptosis and activated cardiomyocyte autophagy, which may be mediated by activation of AMPKa and inhibition of JNK pathways.

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Section: Discussionsupporting

confidence: 62%

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Liang

Qian

Zong

2017

Molecular Medicine Reports

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“…In the present study, the p-JNK levels were significantly elevated after treatment with 250 µM capsaicin, which was correlated with the capsaicin-induced apoptotic effects in all 3 OS cell lines; these data suggest that capsaicin-induced OS cell apoptosis is at least partially involved in activating the JNK signaling pathway. Our results are consistent with those of previous findings that capsaicin could increase JNK phosphorylation and thus promote apoptosis in cancer cells ( 41 , 47 ). Taken together, the findings in the present study strongly suggest that inactivation of ERK1/2 and p38 plays an important role in capsaicin-induced inhibition of proliferation and cell cycle arrest in OS cells, whereas JNK activation participated in capsaicin-induced apoptosis.…”

Section: Discussionsupporting

confidence: 94%

“…The MAPK family plays a critical role in OS cell survival, proliferation and angiogenesis. In addition, some other studies showed that capsaicin could alter the MAPK pathways in cancer cells ( 25 , 41 ). Based on previous studies, we hypothesized that capsaicin may mediate its anti-OS effects by regulating MAPK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Park et al ( 25 ) reported that capsaicin suppressed the phosphorylation of p38 in human AGS gastric cancer cells. However, Liu et al ( 41 ) demonstrated that capsaicin mediated its anticancer effects by activating p38 in human renal carcinoma. In the present study, capsaicin significantly inhibited the phosphorylation of p38 in all 3 OS cell lines, which was also correlated with the capsaicin-induced antiproliferative effects on OS cells.…”

Section: Discussionmentioning

confidence: 99%

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Capsaicin inhibits proliferation and induces apoptosis in osteosarcoma cell lines via the mitogen-activated protein kinase pathway

et al. 2017

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Capsaicin, a pungent molecular compound present in many hot peppers, exerts anticancer activities against various human cancer cell lines by inducing apoptosis. However, the effects of capsaicin on human osteosarcoma (OS) as well as the related mechanisms remain to be fully elucidated. In the present study, the anticancer effects of capsaicin on 3 human OS cell lines (MG63, 143B and HOS) were investigated. Various concentrations of capsaicin (50–300 µM) effectively decreased cell viability in all 3 OS cell lines in a dose-dependent manner. Notably, capsaicin-induced apoptosis was observed when OS cells were treated with relatively high concentrations of capsaicin (starting at 250 µM). In addition, the mitochondrial apoptotic pathway was involved in the capsaicin-induced apoptosis in the OS cells. Meanwhile, our results also indicated that at relatively low concentrations (e.g., 100 µM), capsaicin could inhibit the proliferation, decrease the colony forming ability and induce G0/G1 phase cell cycle arrest of OS cells in a dose-dependent manner. Moreover, our results revealed that the anticancer effects induced by capsaicin on OS cell lines involved multiple MAPK signaling pathways as indicated by inactivation of the ERK1/2 and p38 pathways and activation of the JNK pathway. Furthermore, the results of animal experiments showed that capsaicin inhibited tumor growth in a xenograft model of human OS. In conclusion, these results indicate that capsaicin may exert therapeutic benefits as an adjunct to current cancer therapies but not as an independent anticancer agent.

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“…A correlation between TRPV1 channel expression and patients with glioblastoma multiforme was also reported (Alptekin et al 2015). Involvement of TRPV1 activation on the tumor cell proliferation and ROS production in several cancer types was recently reported (Qian et al 2016;Liu et al 2016). In addition, antioxidant treatments via inhibition of the TRPV1 in the cancer cells decreased oxidative stress (Qian et al 2016;Liu et al 2016).…”

Section: Research Articlementioning

confidence: 87%

Clostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathways

Akyuva¹

2020

Journal of Cellular Neuroscience and Oxidative Stress

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Journal of Cellular Neuroscience and Oxidative Stress is an online journal that publishes original research articles, reviews and short reviews on the molecular basis of biophysical, physiological and pharmacological processes that regulate cellular function, and the control or alteration of these processes by the action of receptors, neurotransmitters, second messengers, cation, anions, drugs or disease. Areas of particular interest are four topics. They are; A-Ion Channels (Na +-K + Channels, Clchannels, Ca 2+ channels, ADP-Ribose and metabolism of NAD + , Patch-Clamp applications) B-Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) C-Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD + on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson's and Alzheimer's diseases) D-Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)

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Capsaicin mediates caspases activation and induces apoptosis through P38 and JNK MAPK pathways in human renal carcinoma

Cited by 51 publications

References 37 publications

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Capsaicin inhibits proliferation and induces apoptosis in osteosarcoma cell lines via the mitogen-activated protein kinase pathway

Clostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathways

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