Mollugin induces apoptosis in human Jurkat T cells through endoplasmic reticulum stress-mediated activation of JNK and caspase-12 and subsequent activation of mitochondria-dependent caspase cascade regulated by Bcl-xL

Kim, Sun Mi; Park, Hae Sun; Jun, Do Youn; Woo, Hyun Ju; Woo, Mi Hee; Yang, Chae Ha; Kim, Young Ho

doi:10.1016/j.taap.2009.08.024

Cited by 41 publications

(25 citation statements)

References 50 publications

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“…Furthermore, treatment with ACDB increased the expression of the upstream protein caspase-9 (10.89 fold) and the cytosolic fraction of cytochrome C (2.04 fold) in JJ012 cells (Figure 5B) as well as cleaved-PARP expression (5.40 fold) (Figure 5B). On the other hand, we continued to determine the involvement of caspase with the specific caspase-3 inhibitor, z-DEVD-FMK, and caspase-9 inhibitor, z-LEHD-FMK [30]. JJ012 cells pretreated with z-DEVD-FMK and z-LEHD-FMK largely diminished ACDB-enhanced cell apoptosis, as shown by the cell cycle assay (Figure 5C).…”

Section: Resultsmentioning

confidence: 99%

A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress

Chen

Lü

et al. 2016

Oncotarget

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Chondrosarcoma is one of the bone tumor with high mortality in respond to poor radiation and chemotherapy treatment. Here, we analyze the antitumor activity of a novel benzofuran derivative, 2-amino-3-(2-chlorophenyl)-6-(4-dimethylaminophenyl)benzofuran-4-yl acetate (ACDB), in human chondrosarcoma cells. ACDB increased the cell apoptosis of human chondrosarcomas without harm in chondrocytes. ACDB also enhanced endoplasmic reticulum (ER) stress, which was characterized by varieties in the cytosolic calcium levels and induced the expression of glucose-regulated protein (GRP) and calpain. Furthermore, the ACDB-induced chondrosarcoma apoptosis was associated with the upregulation of the B cell lymphoma-2 (Bcl-2) family members including pro- and anti-apoptotic proteins, downregulation of dysfunctional mitochondria that released cytochrome C, and subsequent activation of caspases-3. In addition, the ACDB-mediated cellular apoptosis was suppressed by transfecting cells with glucose-regulated protein (GRP) and calpain siRNA or treating cells with ER stress chelators and caspase inhibitors. Interestingly, animal experiments illustrated a reduction in the tumor volume following ACDB treatment. Together, these results suggest that ACDB may be a novel tumor suppressor of chondrosarcoma, and this study demonstrates that the novel antitumor agent, ACDB, induced apoptosis by mitochondrial dysfunction and ER stress in human chondrosarcoma cells in vitro and in vivo.

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Section: Resultsmentioning

confidence: 99%

A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress

Chen

Lü

et al. 2016

Oncotarget

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“…These roots are usually used to treat inflammation of the joints, dysmenorrhea, hematorrhea, hemostasis, and psoriasis. 5,6) Mollugin, the major and index component determining the quality of Rubia cordifolia L., was reported to have several pharmacological effects, such as cytotoxic and anti-tumor activities, 7) anti-platelet aggregation activity, 8) and antiviral activity against hepatitis B virus. 9) Recently, Kim and Jeong reported that mollugin might be a new drug candidate for the treatment of inflammatory diseases, such as colon inflammation and neurodegenerative diseases.…”

mentioning

confidence: 99%

Mollugin Inhibits the Inflammatory Response in Lipopolysaccharide-Stimulated RAW264.7 Macrophages by Blocking the Janus Kinase-Signal Transducers and Activators of Transcription Signaling Pathway

Zhu

Jin

et al. 2013

Biological & Pharmaceutical Bulletin

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Mollugin, a kind of naphthohydroquinone, is a major constituent isolated from Rubia cordifolia L. and demonstrated to possess anti-inflammatory activity in recent reports. However, the effects and mechanism of action of mollugin in inflammation have not been fully defined. The present study was therefore designed to investigate whether mollugin suppresses the inflammatory response in lipopolysaccharide (

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“…The MAPK pathway (JNK, p38 and ERK) is one of the molecular mechanisms to regulate cancer cell activity. Phospho-p38 can induce apoptosis and phospho-ERK can inhibit apoptosis (27)(28)(29). Our results showed that Tan-IIA increased the protein expression levels of p-JNK (especially after 1 h) and p-p38 (especially after 6 h).…”

Section: The Effects Of Tan-iia On the Protein Expression Of Bax Bclmentioning

confidence: 53%

Tanshinone IIA inhibits BT-20 human breast cancer cell proliferation through increasing caspase 12, GADD153 and phospho-p38 protein expression

et al. 2012

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Abstract. Breast cancer is the leading cause of cancer-related deaths in women worldwide. Tanshinone IIA (Tan-IIA) is one of the pure compounds from Salviae miltiorrhizae radix (Danshen). Tan-IIA can inhibit human breast cancer cells but the molecular mechanisms are not well understood. Our previous study showed that Tan-IIA can inhibit hep-J5 human hepatocellular carcinoma cells through the endoplasmic reticulum (ER) stress-induced apoptotic pathway. In the present study, we evaluated the effects of Tan-IIA on BT-20 human breast cancer cells and assessed the involvement of the ER-stress-apoptotic pathway. The cytotoxicity of Tan-IIA in BT-20 cells was measured by the MTT assay. The cell cycles were analyzed by flow cytometry. The expression of ER stress-related proteins in BT-20 cells treated with Tan-IIA were evaluated by western blotting and immunocytochemical staining. These results showed that Tan-IIA can inhibit BT-20 cells and increase the sub-G1 phase in a time-and dose-dependent manner. Tan-IIA could increase the protein expression of caspase 12, GADD153, caspase 3, phospho-JNK, phospho-p38 and Bax, but decreased Bcl-xl and phospho-ERK expression in BT-20 cells. These findings indicate that Tan-IIA possesses therapeutic potential for human breast cancer BT-20 cells; one of the molecular mechanisms may be through inducing ER stress and the MAPK pathway to induce apoptosis and inhibit proliferation.

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Mollugin induces apoptosis in human Jurkat T cells through endoplasmic reticulum stress-mediated activation of JNK and caspase-12 and subsequent activation of mitochondria-dependent caspase cascade regulated by Bcl-xL

Cited by 41 publications

References 50 publications

A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress

A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress

Mollugin Inhibits the Inflammatory Response in Lipopolysaccharide-Stimulated RAW264.7 Macrophages by Blocking the Janus Kinase-Signal Transducers and Activators of Transcription Signaling Pathway

Tanshinone IIA inhibits BT-20 human breast cancer cell proliferation through increasing caspase 12, GADD153 and phospho-p38 protein expression

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