Effects of HIF-1α on human gastric cancer cell apoptosis at different CO2 pressures

Hao, Ya; Yu, Ping; Zhang, Chao; Zeng, Da‐Wu; Shi, Yan; Tang, Bo

doi:10.1007/s10238-008-0023-z

Cited by 10 publications

(7 citation statements)

References 33 publications

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“…Hao et al . reported that exposure of gastric cancer cells to CO 2 pneumoperitoneum significantly induced apoptosis [26]. In the current study, we demonstrate that transcutaneous application of CO 2 to human MFH cells in an engrafted tumor model, upregulated the expression of PGC-1α and TFAM, increased the number of mitochondria, and led to mitochondrial-induced apoptosis.…”

Section: Discussionsupporting

confidence: 66%

Transcutaneous Application of Carbon Dioxide (CO2) Induces Mitochondrial Apoptosis in Human Malignant Fibrous Histiocytoma In Vivo

et al. 2012

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Mitochondria play an essential role in cellular energy metabolism and apoptosis. Previous studies have demonstrated that decreased mitochondrial biogenesis is associated with cancer progression. In mitochondrial biogenesis, peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) regulates the activities of multiple nuclear receptors and transcription factors involved in mitochondrial proliferation. Previously, we showed that overexpression of PGC-1α leads to mitochondrial proliferation and induces apoptosis in human malignant fibrous histiocytoma (MFH) cells in vitro. We also demonstrated that transcutaneous application of carbon dioxide (CO2) to rat skeletal muscle induces PGC-1α expression and causes an increase in mitochondrial proliferation. In this study, we utilized a murine model of human MFH to determine the effect of transcutaneous CO2 exposure on PGC-1α expression, mitochondrial proliferation and cellular apoptosis. PGC-1α expression was evaluated by quantitative real-time PCR, while mitochondrial proliferation was assessed by immunofluorescence staining and the relative copy number of mitochondrial DNA (mtDNA) was assessed by real-time PCR. Immunofluorescence staining and DNA fragmentation assays were used to examine mitochondrial apoptosis. We also evaluated the expression of mitochondrial apoptosis related proteins, such as caspases, cytochorome c and Bax, by immunoblot analysis. We show that transcutaneous application of CO2 induces PGC-1α expression, and increases mitochondrial proliferation and apoptosis of tumor cells, significantly reducing tumor volume. Proteins involved in the mitochondrial apoptotic cascade, including caspase 3 and caspase 9, were elevated in CO2 treated tumors compared to control. We also observed an enrichment of cytochrome c in the cytoplasmic fraction and Bax protein in the mitochondrial fraction of CO2 treated tumors, highlighting the involvement of mitochondria in apoptosis. These data indicate that transcutaneous application of CO2 may represent a novel therapeutic tool in the treatment of human MFH.

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Section: Discussionsupporting

confidence: 66%

Transcutaneous Application of Carbon Dioxide (CO2) Induces Mitochondrial Apoptosis in Human Malignant Fibrous Histiocytoma In Vivo

et al. 2012

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“…[41] Basic research in vitro also demonstrated that CO 2 pneumoperitoneum did not increase the proliferation rate and invading ability of gastric cancer cells. [42,43] …”

Section: Discussionmentioning

confidence: 99%

Comparison of laparoscopy-assisted and open radical gastrectomy for advanced gastric cancer

Hao

Yu²,

Qian³

et al. 2016

Medicine

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Laparoscopy-assisted gastrectomy (LAG) has gained international acceptance for the treatment of early gastric cancer (EGC). However, the use of laparoscopic surgery in the management of advanced gastric cancer (AGC) has not attained widespread acceptance. This retrospective large-scale patient study in a single center for minimally invasive surgery assessed the feasibility and safety of LAG for T2 and T3 stage AGC. A total of 628 patients underwent LAG and 579 patients underwent open gastrectomy (OG) from Jan 2004 to Dec 2011. All cases underwent radical lymph node (LN) dissection from D1 to D2+. This study compared short- and long-term results between the 2 groups after stratifying by pTNM stages, including the mean operation time, volume of blood loss, number of harvested LNs, average days of postoperative hospital stay, mean gastrointestinal function recovery time, intra- and post-operative complications, recurrence rate, recurrence site, and 5-year survival curve. Thirty-five patients (5.57%) converted to open procedures in the LAG group. There were no significant differences in retrieved LN number (30.4 ± 13.4 vs 28.1 ± 17.2, P = 0.43), proximal resection margin (PRM) (6.15 ± 1.63 vs 6.09 ± 1.91, P = 0.56), or distal resection margin (DRM) (5.46 ± 1.74 vs 5.40 ± 1.95, P = 0.57) between the LAG and OG groups, respectively. The mean volume of blood loss (154.5 ± 102.6 vs 311.2 ± 118.9 mL, P < 0.001), mean postoperative hospital stay (7.6 ± 2.5 vs 10.7 ± 3.6 days, P < 0.001), mean time for gastrointestinal function recovery (3.3 ± 1.4 vs 3.9 ± 1.5 days, P < 0.001), and postoperative complications rate (6.4% vs 10.5%, P = 0.01) were clearly lower in the LAG group compared to the OG group. However, the recurrence pattern and site were not different between the 2 groups, even they were stratified by the TNM stage. The 5-year overall survival (OS) rates were 85.38%, 79.70%, 57.81%, 34.60% and 88.31%, 75.49%, 56.84%, 33.08% in patients with stage Ib, IIa, IIb, and IIIa, respectively, in the LAG and OG groups. There were no statistically significant differences in the OS rate for patients with the same TNM stage between the 2 groups. LAG with radical LN dissection is a safe and technically feasible procedure for the treatment of AGC staged below T3.

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“…Bcl-2 and Bax both are members of Bcl-2 family. The former is an anti-apoptosis protein and the latter is a pro-apoptosis protein (20). In the present study, overexpression of GSTM3 downregulated the Bcl-2 expression and upregulated the Bax expression.…”

Section: Discussionmentioning

confidence: 99%

GSTM3 reverses the resistance of hepatoma cells to radiation by regulating the expression of cell cycle/apoptosis-related molecules

et al. 2014

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Radiotherapy (RT) is a major modality of hepatoma treatment. However, liver tumors often acquire radioresistance, which contributes to RT failure. The exact mechanisms of the radioresistance in hepatoma cells are largely unknown. Glutathione S-transferase M3 (GSTM3) is a phase II transferase, however, recent studies have suggested that GSTM3 is a potential tumor suppressor. The purpose of the present study was to investigate the role of GSTM3 in reversing radioresistance, and to explore the molecular mechanism of this in the human radiation-resistant PRF/PLC/5R hepatocellular carcinoma (HCC) cell line. The radioresistant PLC/PRF/5R cells were used as cell model, and were derived from PLC/PRF/5 parental cells using fractionated irradiation. The radiosensitivity of the cells was tested by clonogenic assay and flow cytometry analyses. The expression of B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2), Bax, p21, p27 and p53 was analyzed by quantitative polymerase chain reaction and immunoblotting with or without radiation. The results showed that the expression levels of GSTM3 were significantly lower in the PLC/PRF/5R cells than in the PLC/PRF/5 parental cells. GSTM3 overexpression sensitized the PLC/PRF/5R cells to radiation mainly though induction of apoptosis. According to the evidence from Annexin-V/PI staining, it markedly increased the percentage of apoptotic PRF/PLC/5R cells. The clonogenic assay indicated that GSTM3 significantly decreased the RT survival fraction in PRF/PLC/5R cells. Furthermore, GSTM3 increased the expression of cell cycle- and apoptosis-related genes (Bcl-2, Bax, p21, p27 and p53) in PRF/PLC/5R cells with irradiation. These findings suggest that GSTM3 plays an pivotal role in reversing the radioresistance of HCC and may be a potential target for sensitizing HCC cells to RT. The underlying mechanisms may be linked to the cell cycle arrest and apoptosis facilitation.

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Effects of HIF-1α on human gastric cancer cell apoptosis at different CO2 pressures

Cited by 10 publications

References 33 publications

Transcutaneous Application of Carbon Dioxide (CO2) Induces Mitochondrial Apoptosis in Human Malignant Fibrous Histiocytoma In Vivo

Transcutaneous Application of Carbon Dioxide (CO2) Induces Mitochondrial Apoptosis in Human Malignant Fibrous Histiocytoma In Vivo

Comparison of laparoscopy-assisted and open radical gastrectomy for advanced gastric cancer

GSTM3 reverses the resistance of hepatoma cells to radiation by regulating the expression of cell cycle/apoptosis-related molecules

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