Apoptosis induction associated with the ER stress response through up-regulation of JNK in HeLa cells by gambogic acid

Krajarng, Aungkana; Imoto, Masaya; Tashiro, Etsu; Fujimaki, Takahiro; Shinjo, Satoko; Watanapokasin, Ramida

doi:10.1186/s12906-015-0544-4

Cited by 39 publications

(22 citation statements)

References 37 publications

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“…JNK activation can be induced by both exogenous and endogenous ROS (53). In addition, JNK activation serves a pivotal role in the induction of apoptotic cells (54). In the present study, it was demonstrated that treatment with andrographolide significantly increased the expression levels of phosphorylated JNK in osteosarcoma cells.…”

Section: Discussionsupporting

confidence: 56%

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

Wang

Chen

et al. 2020

Int J Oncol

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Osteosarcoma is the most common primary malignant tumor of the bone and the long-term survival of patients with this disease has remained unsatisfactory over the past several decades. Andrographolide, a traditional drug used in Chinese medicine, has been found to exert a significant antitumor effect against several types of cancer. However, relatively little is known about the effect of andrographolide on osteosarcoma and the underlying mechanisms. In the present study, it was shown that andrographolide inhibited osteosarcoma cell proliferation by arresting the cell cycle at the G2/M phase and increasing caspase-mediated apoptosis. Furthermore, treatment with andrographolide induced JNK activation and increased production of reactive oxygen species (ROS). The andrographolide-triggered apoptosis in osteosarcoma cells was partly abrogated by a JNK inhibitor and completely reversed by a ROS scavenger. Additionally, JNK activation and cell cycle arrest at the G2/M phase were prevented by administration of an ROS scavenger. In vivo, it was also found that andrographolide inhibited tumor growth by increasing the levels of ROS and activating JNK; thus inducing cytotoxicity in primary osteosarcoma cells. Together, the results of the present study suggest that andrographolide caused G2/M arrest and induced cell apoptosis via regulation of the ROS/JNK signaling pathway in osteosarcoma cells. Thus, andrographolide may serve as a promising antitumor therapeutic agent against osteosarcoma.

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Section: Discussionsupporting

confidence: 56%

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

Wang

Chen

et al. 2020

Int J Oncol

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“…Various studies have reported the increased transcriptional activation of DR5 gene by the upregulation of CHOP expression (41)(42)(43)(44)(45), these correlated to the upregulation of CHOP expression in goniothalamin treatment. Another mechanism which is involved in sensitization to TRAIL-induced apoptosis is downregulation of cFLIP and Mcl1.…”

Section: Discussionmentioning

confidence: 99%

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Sophonnithiprasert

Nilwarangkoon

Nakamura

et al. 2015

International Journal of Oncology

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Abstract. The combination of TNF-related apoptosis-inducing ligand (TRAIL) and bioactive compound to enhance apoptosis in TRAIL-resistant cancer is one of cancer treatment strategies. TRAIL possesses the unique capacity to selectively induce apoptosis in cancer cells both in vitro and in vivo with little effect on normal cells. Recent studies have reported that there are many TRAIL-resistant cancers. Thus, bioactive compounds that enhance cytotoxicity of TRAIL would be potential candidates for cancer therapeutic application. This study evaluated the cytotoxic and apoptosis induction upon combined treatment of TRAIL and goniothalamin, the natural styryl-lactone compound extracted from plant Goniothalamus spp., in LoVo cells. The results showed that a combination of goniothalamin and TRAIL enhanced caspase-dependent apoptosis induction in LoVo cells via both death receptor-and mitochondrial-mediated apoptosis pathways. In addition, goniothalamin enhanced TRAIL-induced apoptosis through increased death receptor DR5 expression and decreased anti-apoptotic regulator cFLIP. Interestingly, goniothalamin increased translocation of DR5 to cell surface and consequently contributed to the enhancement of TRAIL-induced apoptosis. In conclusion, this is the first report showing the combined treatment of goniothalamin and TRAIL was able to effectively enhance TRAIL-mediated apoptosis induction in TRAIL-refractory colorectal cancer, LoVo cells. Therefore, this study may offer a strategic cancer treatment against TRAIL-resistant cancers.

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“…In the Hoechst 33342 assay, cells stained by Hoechst33342 were observed by fluorescence microscopy, a classic method to distinguish apoptotic cells, normal cells and necrotic cells (37,38). A small amount of Hoechst 33342 could penetrate the normal cell membranes and emit equivalent dark blue fluorescence after combination with DNA.…”

Section: Discussionmentioning

confidence: 99%

Oridonin induces apoptosis through the mitochondrial pathway in human gastric cancer SGC-7901 cells

Gao

Tan

Zhu

et al. 2016

International Journal of Oncology

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Abstract.Oridonin is one of the most important antitumor active ingredients of Rabdosia rubescens. Recently published studies from our laboratory have demonstrated that oridonin was able to arrest human gastric cancer SGC-7901 cells at G 2 /M phase. However, little is known about inducing apoptosis in gastric cancer. The aim of this study was to investigate the effect of oridonin on antineoplastic capability of SGC-7901 cells and the detailed molecular mechanism of oridoninmediated intrinsic pathway of apoptosis. Cell proliferation was assessed by MTT assay while apoptosis induced by oridonin was determined by Hoechst 33342 staining assay and Annexin V/PI double staining assay. Early apoptotic rate was stained by Annexin V/PI and detected by flow cytometry. Apoptosis pathway was analyzed by western blot analysis of Bcl-2, Bax, cytochrome c and caspase-3 expression. The results showed that oridonin was able to inhibit the SGC-7901 cell proliferation, the 50% growth inhibition (IC 50 ) was 22.74 µM. Oridonin could induce cell apoptosis of SGC-7901 cells and the early apoptotic rates induced by 0, 20, 40, 80 µmol/l oridonin were 1.53±0.67, 3.33±0.29, 84.80±0.82 and 96.43±0.51%, respectively. Western blot analysis revealed that oridonin downregulated Bcl-2 protein (the anti-apoptotic factor) and upregulated Bax protein (pro-apoptotic factor), eventually leading to a reduction in the ratio of Bcl-2/Bax proteins. Furthermore, oridonin induced the release of cytochrome c from the mitochondria to the cytosol and the activation of caspase-3. Taken together, the current study suggested that oridonin induced apoptosis in SGC-7901 cells via the mitochondrial signal pathway, which may represent one of the major mechanisms of oridonin-mediated apoptosis in SGC-7901 cells.

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Apoptosis induction associated with the ER stress response through up-regulation of JNK in HeLa cells by gambogic acid

Cited by 39 publications

References 37 publications

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Oridonin induces apoptosis through the mitochondrial pathway in human gastric cancer SGC-7901 cells

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