Hmgb1 inhibits Klotho expression and malignant phenotype in melanoma cells by activating NF-κB

Xie, Biao; Cao, Ke; Li, Jinjin; Chen, Jia; Tang, Jintian; Chen, Xiang; Xia, Kun; Zhou, Xiao Yan; Cheng, Yan; Zhou, Jianda; Xie, Hui

doi:10.18632/oncotarget.12623

Cited by 19 publications

(12 citation statements)

References 17 publications

(21 reference statements)

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“…miR-22-mimics/inhibitors, REDD1-shRNAs, plasmids for overexpression of REDD1, and negative controls were purchased from GeneChem Biotechnology Company. Cells were transfected as previously described (23)(24)(25). BUC cells were seeded in 6-well plates and allowed to reach 70% confluence after 24 hours.…”

Section: Cell Transfectionmentioning

confidence: 99%

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Zeng

Liu

Cao

et al. 2018

Clinical Cancer Research

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Regulated in development and DNA damage response-1 (REDD1) is a stress-related protein and is involved in the progression of cancer. The role and regulatory mechanism of REDD1 in bladder urothelial carcinoma (BUC), however, is yet unidentified. The expression of REDD1 in BUC was detected by Western blot analysis and immunohistochemistry (IHC). The correlation between REDD1 expression and clinical features in patients with BUC were assessed. The effects of REDD1 on cellular proliferation, apoptosis, autophagy, and paclitaxel sensitivity were determined both and Then the targeted-regulating mechanism of REDD1 by miRNAs was explored. Here the significant increase of REDD1 expression is detected in BUC tissue, and REDD1 is first reported as an independent prognostic factor in patients with BUC. Silencing REDD1 expression in T24 and EJ cells decreased cell proliferation, increased apoptosis, and decreased autophagy, whereas the ectopic expression of REDD1 in RT4 and BIU87 cells had the opposite effect. In addition, the REDD1-mediated proliferation, apoptosis, and autophagy are found to be negatively regulated by miR-22 , which intensify the paclitaxel sensitivity via inhibition of the well-acknowledged REDD1-EEF2K-autophagy axis. AKT/mTOR signaling initially activated or inhibited in response to silencing or enhancing REDD1 expression and then recovered rapidly. Finally, the inhibited REDD1 expression by either RNAi or miR-22 sensitizes BUC tumor cells to paclitaxel in a subcutaneous transplant carcinoma model REDD1 is confirmed as an oncogene in BUC, and antagonizing REDD1 could be a potential therapeutic strategy to sensitize BUC cells to paclitaxel. .

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Section: Cell Transfectionmentioning

confidence: 99%

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Zeng

Liu

Cao

et al. 2018

Clinical Cancer Research

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“…Malignant melanoma (MM) is one of the aggressive skin cancers with a high mortality rate despite its improvements in diagnostic and therapeutic technology [1][2][3]. Although great advance has been achieved in the early diagnosis and treatment, the prognosis of MM paitents remains very poor [4,5].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Loss of miR-494 by exosomes promotes melanoma proliferation and metastasis

Li¹,

Chen²,

Wang³

et al. 2018

Oncotarget

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Previous studies have established that exosomes involve material transport in melanoma. However, the detail molecular mechanisms remain to be elucidated. Here, we aimed to determine the functions of exosome-derived miR-494 in melanoma progress. In this study, we firstly found significantly higher levels of miR-494 in melanoma patients' serum exosomes. miR-494 was upregulated in high-metastaic melanoma cell exosomes while downregulated in cell itself.. Functional studies revealed that decrease exosome production and overexpression of miR-494 significantly inhibited cancer cells proliferation, migration and invasion in vitro. Nude mice experiments confirmed that upregulation miR-494 suppressed tumor growth and metastasis by inhibiting exosomes release in vivo. In conclusion, Exosomal transfer of miR-494 is an alternative modality in the treatment of melanoma.

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“…Malignant melanoma (MM), an aggressive skin malignancy, is the fifth most common malignant tumor in men and the seventh most common malignant tumor in women [ 1 , 2 ]. Recent studies showed that the incidence of MM has increased by 3.1% per year [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

microRNA-33a-5p increases radiosensitivity by inhibiting glycolysis in melanoma

Cao

Chen

et al. 2017

Oncotarget

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Glycolysis was reported to have a positive correlation with radioresistance. Our previous study found that the miR-33a functioned as a tumor suppressor in malignant melanoma by targeting hypoxia-inducible factor1-alpha (HIF-1α), a gene known to promote glycolysis. However, the role of miR-33a-5p in radiosensitivity remains to be elucidated. We found that miR-33a-5p was downregulated in melanoma tissues and cells. Cell proliferation was downregulated after overexpression of miR-33a-5p in WM451 cells, accompanied by a decreased level of glycolysis. In contrast, cell proliferation was upregulated after inhibition of miR-33a-5p in WM35 cells, accompanied by increased glycolysis. Overexpression of miR-33a-5p enhanced the sensitivity of melanoma cells to X-radiation by MTT assay, while downregulation of miR-33a-5p had the opposite effects. Finally, in vivo experiments with xenografts in nude mice confirmed that high expression of miR-33a-5p in tumor cells increased radiosensitivity via inhibiting glycolysis. In conclusions, miR-33a-5p promotes radiosensitivity by negatively regulating glycolysis in melanoma.

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Hmgb1 inhibits Klotho expression and malignant phenotype in melanoma cells by activating NF-κB

Abstract: ABSTRACT

Cited by 19 publications

References 17 publications

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

WITHDRAWN: Loss of miR-494 by exosomes promotes melanoma proliferation and metastasis

microRNA-33a-5p increases radiosensitivity by inhibiting glycolysis in melanoma

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