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

Oncology Reports
Yulan ZhenJingfu Chen

Abstract

Hydrogen sulfide (H2S) participates in multifarious physiological and pathophysiologic progresses of cancer both in vitro and in vivo. We have previously demonstrated that exogenous H2S promoted liver cancer cells proliferation/anti‑apoptosis/angiogenesis/migration effects via amplifying the activation of NF-κB pathway. However, the effects of H2S on cancer cell proliferation and apoptosis are controversial and remain unclear in C6 glioma cells. The present study investigated the effects of exogenous H2S 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 H2S) 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 Kit-8 (CCK-8). 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 decrease...Continue Reading

References

Feb 3, 1998·The American Journal of Gastroenterology·J LevineM D Levitt
Mar 19, 1999·Molecular and Cellular Biology·H J Schaeffer, M J Weber
Mar 10, 2001·Nature·L Chang, M Karin
Jul 27, 2002·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Tong WuA Jake Demetris
Nov 1, 2002·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Rui Wang
Jun 10, 2004·Microbiology and Molecular Biology Reviews : MMBR·Philippe P Roux, John Blenis
May 15, 2007·Oncogene·A G TurjanskiJ S Gutkind
Jul 10, 2007·Acta Neuropathologica·David N LouisPaul Kleihues
Aug 26, 2009·Neurochemistry International·Boon Hian TanJin-Song Bian
Oct 7, 2009·Antioxidants & Redox Signaling·Qiuhui CaoRui Wang
Feb 27, 2010·Cell Biology International·Wen-Jie CaiYi-Chun Zhu
May 28, 2010·Toxicology and Industrial Health·Kaye H KilburnMichael R Gray
Jul 9, 2010·Lancet Neurology·Michael JansenDavid N Louis
Nov 16, 2010·International Journal of Toxicology·Tee L Guidotti
Feb 1, 2011·Inflammation & Allergy Drug Targets·Weifang RongDavid Grundy
Aug 31, 2011·Free Radical Biology & Medicine·Emanuela PupoLuca Munaron
Dec 15, 2012·Cancer Genetics·McKinsey L Goodenberger, Robert B Jenkins
Jul 10, 2013·Proceedings of the National Academy of Sciences of the United States of America·Csaba SzaboMark R Hellmich
Aug 29, 2013·Clinical & Developmental Immunology·Jun WeiAmy Heimberger
Dec 21, 2013·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·Daofang DingYuelong Cao
Mar 25, 2014·Research in Veterinary Science·Kyoung-Won SeoHwa-Young Youn
Mar 29, 2014·Cancer Cell International·Xing WuLie-Ming Lou
Sep 18, 2014·ACS Chemical Neuroscience·Xingzhou Zhang, Jin-Song Bian
Dec 2, 2014·Molecular Medicine Reports·Bicheng ZhangJianfei Gao
Dec 22, 2014·Reviews in the Neurosciences·Wen-Lin ChenXiao-Qing Tang

❮ Previous
Next ❯

Citations

Mar 20, 2016·Pancreatology : Official Journal of the International Association of Pancreatology (IAP) ... [et Al.]·Sooyeon LeeKi Baik Hahm
Jan 3, 2020·DNA and Cell Biology·Na YangQinhui Tuo
Jul 20, 2016·International Journal of Molecular Medicine·Xiaoming YuYu Zhao
Dec 27, 2019·European Journal of Medicinal Chemistry·Haonan LiDahong Li
Sep 10, 2021·Antioxidants & Redox Signaling·Elise MalardLaurent Chatre

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Angiogenesis Inhibitors to Treat Cancer

Cancer treatments including angiogenesis inhibitors prevent tumor cells from receiving nutrients and oxygen. Here is the latest research on angiogenesis inhibitors for the treatment of cancer.

Cell Signaling & Cancer Epigenetics (Keystone)

Epigenetic changes are present and dysregulated in many cancers, including DNA methylation, non-coding RNA segments and post-translational protein modifications. This feed covers the latest research on signaling and epigenetics in cell growth and cancer.

Cancer Epigenetics & Methyl-CpG (Keystone)

Epigenetic changes are present and dysregulated in many cancers, including DNA methylation, non-coding RNA segments and post-translational protein modifications. Here is the latest research on cancer epigenetics and methyl-CpG binding proteins including ZBTB38.

Cancer Epigenetics

Epigenetic changes are present and dysregulated in many cancers, including DNA methylation, non-coding RNA segments and post-translational protein modifications. The epigenetic changes may or may not provide advantages for the cancer cells. Here is the latest research on cancer epigenetics.

Cancer Epigenetics (Keystone)

Epigenetic changes are present and dysregulated in many cancers, including DNA methylation, non-coding RNA segments and post-translational protein modifications. The epigenetic changes may or may not provide advantages for the cancer cells. Here is the latest research on cancer epigenetics.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Cancer Epigenetics & Metabolism (Keystone)

Epigenetic changes are present and dysregulated in many cancers, including DNA methylation, non-coding RNA segments and post-translational protein modifications. The epigenetic changes may or may not provide advantages for the cancer cells. This feed focuses on the relationship between cell metabolism, epigenetics and tumor differentiation.