mRNA Expression of Bax, Bcl-2, p53, Cathepsin B, Caspase-3 and Caspase-9 in the HepG2 Cell Line Following Induction by a Novel Monoclonal Ab Hep88 mAb: Cross-Talk for Paraptosis and Apoptosis

Mitupatum, Thantip; Aree, Kalaya; Kittisenachai, Suthathip; Roytrakul, Sittiruk; Puthong, Songchan; Kangsadalampai, Sasichai; Rojpibulstit, Panadda

doi:10.7314/apjcp.2016.17.2.703

Cited by 59 publications

(31 citation statements)

References 31 publications

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“…Recently, researchers found that Hep88 monoclonal antibodies can inhibit HepG2 cell lines and achieve antitumor effects. For these findings, Hep88 played its role by promoting the expression of p53, caspase 3, caspase 9, and apoptotic Bax proteins . The results implied that caspase 3 was very important for apoptosis of HepG2 cells, which agreed with this experiment.…”

Section: Discussionsupporting

confidence: 87%

Hepatic Microwave Ablation–Induced Tumor Destruction and Animal End Point Survival Can Be Improved by Suppression of Heat Shock Protein 90

Zhai

Zhou

Dou

et al. 2019

J of Ultrasound Medicine

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Objectives-To investigate the effect of heat shock protein 90 (HSP90) modulation on tumor necrosis, apoptosis, tumor growth delay, and end point survival by combining microwave ablation (MWA) with an HSP90 inhibitor in a nude mouse model.Methods-This study was approved by the Ethics Committee. Forty mice with HepG2 subcutaneous xenograft tumors (10 AE 1 mm) were randomized into 4 groups: (1) no treatment, (2) MWA only, (3) the HSP90 inhibitor ganetespib only, and (4) ganetespib combined with MWA. Tumors were harvested 24 hours after treatment, and gross coagulation diameters were measured. The effect of ganetespib on HSP90 and caspase 3 expression in the periablational rim was assessed. Another 40 mice with the same tumors and groupings were observed after treatment. Tumor growth curve and Kaplan-Meier survival analyses were performed with a tumor diameter of 2.2 cm and 40 days of survival as the defined survival end points.Results-Combination treatment significantly increased the coagulation size compared to tumors treated with MWA or ganetespib alone (P < 0.05). The combination of MWA and ganetespib decreased HSP90 expression and increased cleaved caspase 3 expression 24 hours after treatment. Compared with MWA or ganetespib only, combination treatment could lengthen the end point survival and reduce the tumor growth rate.Conclusions-Modulation of HSP production can improve MWA-induced tumor apoptosis and destruction, reduce residual tumor growth rates, and prolong end point survival.

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Section: Discussionsupporting

confidence: 87%

Hepatic Microwave Ablation–Induced Tumor Destruction and Animal End Point Survival Can Be Improved by Suppression of Heat Shock Protein 90

Zhai

Zhou

Dou

et al. 2019

J of Ultrasound Medicine

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“…To further explore the mechanism of miR-499-5p in H/R-induced H9c2 cells, the levels of related apoptotic proteins were determined by western blot. Bcl-2, Bax and caspase-3 are key regulators of apoptosis, and apoptosis mediated by the dysregulation of such three genes underlies a plethora of diseases (Fong et al 2017 ; Mitupatum et al 2016 ). Bcl-2 and Bax are important genes in Bcl-2 gene family, and Bcl-2 inhibits apoptosis, while Bax promotes apoptosis.…”

Section: Discussionmentioning

confidence: 99%

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Shi

Yun-feng²,

Niu³

et al. 2019

Biotechnol Lett

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Objective MiR-499 has been reported to be expressed only in cardiomyocytes, and its expression would increase after acute myocardial infarction (AMI). miR-499 plays a role in the process of cardiomyocytes injury induced by hypoxia/reoxygenation (H/R), however, it still remains unclear. Results Hypoxia inhibited miR-499-5p expression and H/R induced apoptosis. SOX6 was a target gene of miR-499-5p, and high expression of miR-499-5p inhibited the expression of SOX6. MiR-499-5p reduced H9c2 cells injury by inhibiting the expression of SOX6, overexpression of which could reverse the effect of miR-499-5p on H9c2 cells. MiR-499-5p inhibited the levels of LDH and MDA, while overexpression of miR-499-5p inhibited H/R-induced cell apoptosis. MiR-499-5p could up-regulate the level of Bcl-2 and down-regulate the expression levels of Bax and caspase-3. However, SOX6 partially reversed these effects of miR-499-5p. Conclusion We proved that miR-499-5p inhibited H/R-induced cardiomyocytes injury by targeting SOX6. Our results suggested that miR-499-5p/SOX6 pathway may present a potential therapeutic target for the treatment of AMI.

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“…Inhibition of Caspase-3 expression can effectively prevent cell apoptosis [29]. Activated Caspase-9 can effectively incise and activate downstream Caspase-3 to induce cell apoptosis [30]. Apoptotic signals stimulated by death receptor and its ligand system are transduced to regulatory Caspase-8 which then activates the effector Caspases to induce cell apoptosis [31].…”

Section: Discussionmentioning

confidence: 99%

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Zhao

Tang

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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This study aimed to investigate the effect of Junduqing extractive on proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma (NPC) cells and the involved mechanism. Junduqing extractive was prepared. CCK-8 assay found that IC50 of Junduqing extractive in HNE-1 cells was 2.99 mg/ml, so its concentration of 1.0, 2.0 and 3.0 mg/ml was selected to perform the following experiments. HNE-1, HNE-2 and HONE1 cells were then divided into four groups: (1) Control (no treatment); (2) 1.0 mg/ml (1.0 mg/ml Junduqing); (3) 2.0 mg/ml (2.0 mg/ml Junduqing) and (4) 3.0 mg/ml (3.0 mg/ml Junduqing). Cell viability, apoptosis, migration and invasion were examined by CCK-8 assay, annexin V-FITC/PI staining, scratch wound assay and transwell assay, respectively. Compared with the control group, the viability, migration rates and invasive capacity of HNE-1, HNE-2 and HONE1 cells with Junduqing treatments decreased significantly. Higher concentration of Junduqing extractive caused lower viability, smaller migration rates and weaker invasive capacity. Compared with the control group, the apoptosis of HNE-1, HNE-2 and HONE1 cells after treatment with 2.0 and 3.0 mg/ml of Junduqing extractive increased remarkably. Levels of Bcl-xL, Mcl-1, Caspase-3, Caspase-8 and Caspase-9 were examined by western blotting. Compared with the control group, the expression of Bcl-xL and Mcl-1 and the expression of Caspase-3, Caspase-8 and Caspase-9 in HNE-1, HNE-2 and HONE1 cells were significantly downregulated and up-regulated, respectively, after treatment with Junduqing extractive. In conclusion, Junduqing extractive could inhibit the proliferation, migration and invasion, and promote the apoptosis of human NPC cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9.

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mRNA Expression of Bax, Bcl-2, p53, Cathepsin B, Caspase-3 and Caspase-9 in the HepG2 Cell Line Following Induction by a Novel Monoclonal Ab Hep88 mAb: Cross-Talk for Paraptosis and Apoptosis

Cited by 59 publications

References 31 publications

Hepatic Microwave Ablation–Induced Tumor Destruction and Animal End Point Survival Can Be Improved by Suppression of Heat Shock Protein 90

Hepatic Microwave Ablation–Induced Tumor Destruction and Animal End Point Survival Can Be Improved by Suppression of Heat Shock Protein 90

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

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