Hydrogen sulfide induces human colon cancer cell proliferation: Role of Akt, ERK and p21

Cai, Wenjie; Wang, Ming‐Jie; Ju, Liu; Wang, Cheng; Zhu, Yi‐Chun

doi:10.1042/cbi20090368

Cited by 205 publications

(182 citation statements)

References 34 publications

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“…In recent years, more and more attention is paid to H 2 S for its extensive physiological and pathophysiological properties on cancer progresses. Some findings from in vivo and in vitro studies showed that H 2 S is beneficial for cancer cell growth, proliferation, migration and invasion (24)(25)(26)(27)(28)(29)(30), owing to its vascular relaxant and angiogenesis effects. H 2 S promotes the supply of nutrients and blood to the tumor cells and tissues (24).…”

Section: Introductionmentioning

confidence: 99%

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

et al. 2015

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Abstract. Hydrogen sulfide (H 2 S) participates in multifarious physiological and pathophysiologic progresses of cancer both in vitro and in vivo.We have previously demonstrated that exogenous H 2 S promoted liver cancer cells proliferation/anti-apoptosis/angiogenesis/migration effects via amplifying the activation of NF-κB pathway. However, the effects of H 2 S on cancer cell proliferation and apoptosis are controversial and remain unclear in C6 glioma cells. The present study investigated the effects of exogenous H 2 S on cancer cells growth via activating p38 MAPK/ERK1/2-COX-2 pathways in C6 glioma cells. C6 glioma cells were treated with 400 µmol/l NaHS (a donor of H 2 S) for 24 h. The expression levels of phosphorylated (p)-p38 MAPK, total (t)-p38 MAPK, p-ERK1/2, t-ERK1/2, cyclooxygenase-2 (COX-2) and caspase-3 were measured by western blotting assay. Cell viability was detected by Cell Counting . Apoptotic cells were observed by Hoechst 33258 staining assay. Cell proliferation was directly detected under fully automatic inverted microscope. Exposure of C6 glioma cells to NaHS resulted in cell proliferation, as evidenced by an increase in cell viability. In addition, NaHS treatment reduced apoptosis, as indicated by the decreased apoptotic percentage and the cleaved caspase-3 expression. Importantly, exposure of the cells to NaHS increased the expression levels of p-p38 MAPK, p-ERK1/2 and COX-2. Notably, co-treatment of C6 glioma cells with 400 µmol/l NaHS and AOAA (an inhibitor of CBS) largely suppressed the above NaHS-induced effects. Combined treatment with NaHS and SB203580 (an inhibitor of p38 MAPK) or PD-98059 (an inhibitor of ERK1/2) resulted in the synergistic reduction of COX-2 expression and increase of caspase-3 expression, a decreased number of apoptotic cells, along with decreased cell viability. Combined treatment with NS-398 (an inhibitor of COX-2) and NaHS also resulted in the synergistic increase of caspase-3, a decreased in the number of apoptotic cells and the decrease in cell viability. The findings of the present study provide novel evidence that p38 MAPK/ERK1/2-COX-2 pathways are involved in NaHS-induced cancer cell proliferation and anti-apoptosis in C6 glioma cells.

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Section: Introductionmentioning

confidence: 99%

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

et al. 2015

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“…Until now, investigations in cancer research have mainly focused on the effects of H 2 S on proliferation and survival of cancer cells (8)(9)(10)(11). However, controversial results exist, as evidenced by the reported increased (8) or decreased (9) proliferation of colon cancer cells following NaHS treatment.…”

Section: Introductionmentioning

confidence: 98%

“…However, controversial results exist, as evidenced by the reported increased (8) or decreased (9) proliferation of colon cancer cells following NaHS treatment. A study showed that H 2 S derived from NaHS may confer intrinsic radioresistant properties to cancer cells (12).…”

Section: Introductionmentioning

confidence: 99%

A Fast Hydrogen Sulfide–Releasing Donor Increases the Tumor Response to Radiotherapy

Preter

Deriemaeker

Danhier

et al. 2016

Molecular Cancer Therapeutics

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Hydrogen sulfide (H 2 S) is the last gaseous transmitter identified in mammals, and previous studies have reported disparate conclusions regarding the implication of H 2 S in cancer progression. In the present study, we hypothesized that sodium hydrosulfide (NaHS), a fast H 2 S-releasing donor, might interfere with the mitochondrial respiratory chain of tumor cells, increase tumor oxygenation, and potentiate the response to irradiation. Using electron paramagnetic resonance (EPR) oximetry, we found a rapid increase in tumor pO 2 after NaHS administration (0.1 mmol/kg) in two human tumor models (breast MDA-MB-231 and cervix SiHa), an effect that was due to a decreased oxygen consumption and an increased tumor perfusion. Tumors irradiated 15 minutes after a single NaHS administration were more sensitive to irradiation compared with those that received irradiation alone (increase in growth delay by 50%). This radiosensitization was due to the oxygen effect, as the increased growth delay was abolished when temporarily clamped tumors were irradiated. In contrast, daily NaHS injection (0.1 mmol/kg/ day for 14 days) did not provide any effect on tumor growth in vivo. To understand these paradoxical data, we analyzed the impact of external factors on the cellular response to NaHS. We found that extracellular pH had a dramatic effect on the cell response to NaHS, as the proliferation rate (measured in vitro by BrdU incorporation) was increased at pH ¼ 7.4, but decreased at pH ¼ 6.5. Overall, our study highlights the complex role of environmental components in the response of cancer cells to H 2 S and suggests a new approach for the use of H 2 S donors in combination with radiotherapy. Mol Cancer Ther; 15(1); 154-61. Ó2015 AACR.

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“…Studies indicate that administer of exogenous NaHS or production of endogenous H 2 S induce the proliferation of human colon cancer HCT116 cells and human hepatocellular carcinoma cells [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of cystathionine-γ-lyase/H₂S system inhibits cell growth in human breast cancer MDA-MB-231 cells

You

et al. 2017

BIO Web Conf.

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Abstract.Hydrogen sulfide (H 2 S), as the third gasotransmitter, plays important roles in cancer biological processes. Endogenous H 2 S can possess pro-cancer functions. Cystathionine-γ-lyase (CSE), one of main metabolic enzymes synthesizing H 2 S, possesses important roles in the development and progression of cancer. In the present study, the roles of C SE/H 2 S system in human breast cancer cells were investigated. It was observed that CSE was expressed in human breast cancer MDA-MB-231 cells and inhibition of endogenous CSE/H 2 S significantly reduced the cell viability and inhibited cell growth and proliferation in MDA-MB-231 cells. Meanwhile, CSE knockdown induced apoptosis of MDA-MB-231 cells and inhibited migration of MDA-MB-231. In conclusion, CSE/H 2 S system possesses important roles in human breast cancer cells.

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Hydrogen sulfide induces human colon cancer cell proliferation: Role of Akt, ERK and p21

Cited by 205 publications

References 34 publications

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

A Fast Hydrogen Sulfide–Releasing Donor Increases the Tumor Response to Radiotherapy

Down-regulation of cystathionine-γ-lyase/H₂S system inhibits cell growth in human breast cancer MDA-MB-231 cells

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Hydrogen sulfide induces human colon cancer cell proliferation: Role of Akt, ERK and p21

Cited by 205 publications

References 34 publications

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

A Fast Hydrogen Sulfide–Releasing Donor Increases the Tumor Response to Radiotherapy

Down-regulation of cystathionine-γ-lyase/H2S system inhibits cell growth in human breast cancer MDA-MB-231 cells

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Down-regulation of cystathionine-γ-lyase/H₂S system inhibits cell growth in human breast cancer MDA-MB-231 cells