Hydrogen sulfide (H2S)/cystathionine γ-lyase (CSE) pathway contributes to the proliferation of hepatoma cells

Effect of integrin receptor-targeted liposomal paclitaxel for hepatocellular carcinoma targeting and therapy

“…The nude mouse HCC xenograft models were divided into four groups. Tumor volume (mm 3 ) was measured with vernier calipers, and when the tumors reached a volume of 100-200 mm 3 , the mice were administered with PBS, free PTX, LP-PTX or RGD-LP-PTX once every other day for 10 days (total, 10 mg/kg), via tail vein injection. Tumor volumes were also measured every other day.…”

“…According to 2013 statistics, >80% of HCC cases occur in developing countries, 55% of which occur in China (2). No effective therapeutic treatment is currently available, particularly when HCC is diagnosed at an advanced stage (3). Surgical excision is always the primary choice in the clinical treatment of HCC; however, total resection of the tumor is typically not possible, therefore, surgical treatment is supplemented with radiotherapy and chemotherapy to kill the remaining tumor cells (4).…”

The role of hydrogen sulfide in aging and age-related pathologies

“…Hydrogen sulfide attenuates DNA damage in human endothelial cells and fibroblasts by increasing MEK1 S-sulfhydration, ERK1/2 and PARP-1 activity leading to the activation of DNA damage repair mechanisms and protection from cellular senescence [86]. The CSE/H 2 S pathway is important in genome stability and cell proliferation, as its inhibition in hepatoma cells decreased their proliferation, enhanced ROS production and mitochondrial disruption, pronounced DNA damage and increased apoptosis [87]. Proliferation was decreased due to downregulation of ERK1/2 activity [87].…”

“…The CSE/H 2 S pathway is important in genome stability and cell proliferation, as its inhibition in hepatoma cells decreased their proliferation, enhanced ROS production and mitochondrial disruption, pronounced DNA damage and increased apoptosis [87]. Proliferation was decreased due to downregulation of ERK1/2 activity [87]. The increased apoptosis after H 2 S signal inhibition was associated with the activation of p53, p21, Bax and other pro-apoptotic factors [87].…”

“…Proliferation was decreased due to downregulation of ERK1/2 activity [87]. The increased apoptosis after H 2 S signal inhibition was associated with the activation of p53, p21, Bax and other pro-apoptotic factors [87]. Thus, both high [76] as well as low H 2 S levels [87] can induce apoptosis.…”