Inducible HSP70 antagonizes cisplatin‑induced cell apoptosis through inhibition of the MAPK signaling pathway in HGC‑27 cells

Sheng, Lili; Tang, Tuo; Liu, Yinhua; Ma, Yunfei; Wang, Ziqian; Hong, Tao; Zhang, Yao; Zhou, Qi

doi:10.3892/ijmm.2018.3789

Cited by 13 publications

(13 citation statements)

References 28 publications

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“…The present study demonstrated that HSP70 was elevated by CSE treatment in the mitochondrial fraction of HL-60 cells exposed to cisplatin. These results are supported by previous reports showing reduction of HSP70 enhances cisplatin-induced apoptosis in HGC-27 gastric cancer cells and A529 lung adenocarcinoma cells, as well as accumulation of HSP70 inhibits heat shock-induced apoptosis in HL-60 cells [57][58][59]. In relation to these findings, it is of interest that we observed that cisplatin-induced release of cytochrome c from mitochondria and compromised mitochondrial function were reversed by CSE.…”

supporting

confidence: 92%

Chlorella sorokiniana Extract Prevents Cisplatin-Induced Myelotoxicity In Vitro and In Vivo

Lin

Chuang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Cisplatin chemotherapy causes myelosuppression and often limits treatment duration and dose escalation in patients. Novel approaches to circumvent or lessen myelotoxicity may improve clinical outcome and quality of life in these patients. Chlorella sorokiniana (CS) is a freshwater unicellular green alga and exhibits encouraging efficacy in immunomodulation and anticancer in preclinical studies. However, the efficacy of CS on chemoprotection remains unclear. We report here, for the first time, that CS extract (CSE) could protect normal myeloid cells and PBMCs from cisplatin toxicity. Also, cisplatin-induced apoptosis in HL-60 cells was rescued through reservation of mitochondrial function, inhibition of cytochrome c release to cytosol, and suppression of caspase and PARP activation. Intriguingly, cotreatment of CSE attenuated cisplatin-evoked hypocellularity of bone marrow in mice. Furthermore, we observed the enhancement of CSF-GM activity in bone marrow and spleen in mice administered CSE and cisplatin, along with increased CD11b levels in spleen. In conclusion, we uncovered a novel mechanism of CSE on myeloprotection, whereby potentially supports the use of CSE as a chemoprotector against cisplatin-induced bone marrow toxicity. Further clinical investigation of CSE in combination with cisplatin is warranted.

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supporting

confidence: 92%

Chlorella sorokiniana Extract Prevents Cisplatin-Induced Myelotoxicity In Vitro and In Vivo

Lin

Chuang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…accumulating evidence has indicated an important role of the Pi3K/aKT signaling pathway in osteosarcoma (11,34,35); Pi3K/aKT signaling modulates the proliferation, invasion, migration and apoptosis of osteosarcoma cell lines (36)(37)(38)(39)60). Previous studies revealed that alantolactone is a specific inhibitor in several diseases via the Pi3K/aKT signaling pathway (7,8).…”

Section: Discussionmentioning

confidence: 99%

Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

et al. 2019

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osteosarcoma is the most common type of malignant bone cancer and results in cancer-related deaths among adolescents. alantolactone (alT) demonstrates antitumor properties in various diseases; however, its potential role in osteosarcoma is relatively unclear. The aim of the present study was to evaluate the effect of alT on osteosarcoma. alT significantly decreased the viability of U2OS and HOS osteosarcoma cell lines. Cells flow cytometry assay and Hoechst 33258 staining assay revealed that ALT significantly increased the proportion of apoptotic u2oS cells. in addition, wound healing and Transwell invasion assays demonstrated that the invasion and migration of osteosarcoma were markedly reduced upon alT treatment. it was hypothesized that the antitumor functions of alT are mediated through inhibition of the Pi3K/aKT signaling pathway. in conclusion, the results of the present study confirmed the inhibition of ALT on osteosarcoma cells via downregulation of Pi3K/aKT signaling pathways, suggesting alT as a potential therapeutic candidate for osteosarcoma.

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“…The MAPK pathway, known as a cascade of protein kinases, is closely associated with the tumorigenesis in multiple malignancies. [50][51][52] The activation of MAPK pathway could stimulate various oncogenic systems including EMT, which transferred epithelial characteristics into mesenchymal phenotype, finally leading tumors getting migratory and invasive features. 53 Consistently, our study also demonstrated that overexpression of CIC inhibited the proliferative and invasion of RCC cells in vivo through suppressing the activation of MAPK pathway, which indicated that MAPK pathway might be involved in the regulation of miR-106b/CIC axis during proliferation and metastasis in RCC progression.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-106b promotes proliferation and invasion by targeting Capicua through MAPK signaling in renal carcinoma cancer</p>

Miao¹,

Shu²,

Zhuang³

et al. 2019

OTT

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Background: miR-106b has been reported to play a vital role in pathogenesis of some types of cancer, whilst the role of miR-106b in renal carcinoma cancer (RCC) remains unknown. Purpose: The objective of this study was to identify the mechanism of miR-106b regulating the progression of renal carcinoma. Method: The expression of miR-106b was analyzed in RCC cell lines, RCC and adjacent normal renal tissues through qRT-PCR assays. Target mRNA of miR-106b was predicted with databases and verified by luciferase reporter assays. And the effects of miR-106b or targeted mRNA on cell proliferation, invasion, the process of epithelial-mesenchymal transitions (EMTs) were assessed in vitrothrough CCK-8, transwell cell invasion assays, qRT-PCR and Western blotting assays respectively. In addition, the effects of miR-106b on the growth of xenografts mice were analyzedin vivo. Results: The results demonstrated that miR-106b was significantly increased both in RCC tissues and cell lines. Luciferase reporter assays revealed that miR-106b inhibited Capicua expression by targeting its 3ʹ-UTR sequence. And miR-106b promoted cell proliferation, invasion, EMT progression in RCC cellin vitro, as well as promoted the tumor growth of 786-O cells derived xenografts mice. Additionally, loss of Capicua promoted the activation of MAPK signaling pathway. Conclusion: The study suggested that miR-106b regulated RCC progression through MAPK signaling pathway partly by targeting Capicua, which might provide valuable evidence for therapeutic target development of RCC.

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Inducible HSP70 antagonizes cisplatin‑induced cell apoptosis through inhibition of the MAPK signaling pathway in HGC‑27 cells

Cited by 13 publications

References 28 publications

Chlorella sorokiniana Extract Prevents Cisplatin-Induced Myelotoxicity In Vitro and In Vivo

Chlorella sorokiniana Extract Prevents Cisplatin-Induced Myelotoxicity In Vitro and In Vivo

Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

<p>miR-106b promotes proliferation and invasion by targeting Capicua through MAPK signaling in renal carcinoma cancer</p>

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