<i>MIR34A</i>regulates autophagy and apoptosis by targeting<i>HMGB1</i>in the retinoblastoma cell

Liu, Ke; Huang, Jun; Xie, Min; Yu, Yan; Zhu, Shan; Kang, Rui; Cao, Lizhi; Tang, Daolin; Duan, Xuanchu

doi:10.4161/auto.27418

Cited by 120 publications

(112 citation statements)

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“…Finally, a total expression score was given ranging from 0 to 12. Based on the analysis, HMGBI expression was categorized in advance into two groups: low-level HMGBI expression (score 0-3) and highlevel HMGBI expression (score [4][5][6][7][8][9][10][11][12] …”

Section: Quantification Ofprotein Expressionmentioning

confidence: 99%

“…Knockdown of HMGBI inhibits proliferation, migration and invasion of cancer cells through the VEGF-C (4) and NF-KB pathway (7), whereas ectopic expression of HMGB 1 promotes cell growth by suppressing BTB-induced cell death (8) and cell migration by epigenetic silencing of semaphorin 3A (9), decreases Bax and p53 expression and enhances the expression of Bcl-xL, Bcl-2, CyclinDl and NF-KB via activation of the FAK/PI3K/mTOR pathway (8). In addition, extracellular HMGB 1 subsequently enhances resistance to the P-gp-related drugs (adriamycin and vincristine) (10), while knockdown of HMGB 1 restores chemosensitivity and tumor cell death (11).…”

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confidence: 99%

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Clinical Significance of HMGB1 Expression in Human Gastric Cancer

Zhang

et al. 2014

Int J Immunopathol Pharmacol

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High mobility group box 1 (HMGB1) has been proved to be implicated in a variety of cell physiological and pathological behaviors including immune response, inflammation and cancer. Accumulating evidence suggests that HMGB1 plays a critical role in the development and progression of multiple malignancies. However, the clinical significance and prognosis of HMGB1 expression in some cancers remain controversial. The present study aimed to investigate whether overexpression of HMGB1 is an independent prognostic factor in patients with gastric cancer. The correlation of HMGB1 expression with clinicopathologic characteristics and prognosis was assessed by immunohistochemical assay through tissue microarray procedure in 50 primary gastric cancer cases. Our results indicated that the positive expression of HMGB1 was significantly increased in the nucleus of gastric cancer tissues compared with the adjacent non-cancerous tissues (ANCT) (64.0% vs 44.0%, P=0.025), but was not linked to the clinicopathologic features, including the TNM stage (P=0.533) and metastatic lymph node (P=0.771), in patients with gastric cancer. Kapalan-Meier and log-rank analysis demonstrated that overexpression of HMGB1 did not exert significant impact on the overall survival of patients with gastric cancer (P=0.805). Furthermore, Cox regression analysis showed that high HMGB1 protein expression did not represent an independent risk factor for patients with gastric cancer (P=0.677). Taken together, our findings suggest that high expression of HMGB1 is not correlated with the clinicopathologic characteristics of gastric cancer, and can not serve as an independent prognostic biomarker for patients with gastric cancer.

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Section: Quantification Ofprotein Expressionmentioning

confidence: 99%

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confidence: 99%

Clinical Significance of HMGB1 Expression in Human Gastric Cancer

Zhang

et al. 2014

Int J Immunopathol Pharmacol

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“…23,24 miR-34a inhibits autophagy and enhances chemotherapy-induced apoptosis in the retinoblastoma cell through HMGB1. 25 The miR-15a/107 group of miRNA contains a series of miRNAs, including miR-15a, miR-15b, miR-16, miR-103 and miR-107 family. MiR-15a and miR-16 form 2 different clusters in mammals and these 2 miRNAs are found to be frequently deleted or downregulated in many types of cancers, including chronic lymphocytic leukemia (CLL), colorectal cancer, squamous-cell carcinoma, ovarian cancer and prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-15a and miR-16 induce autophagy and enhance chemosensitivity of Camptothecin

Huang

Qiu

et al. 2015

Cancer Biology & Therapy

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Abbreviations: BAFA1, bafilomycin A1; CPT, Camptothecin; miRNA, microRNA; LC3, microtubule-associated protein 1 light chain 3; mTOR, mechanistic target of rapamycin; Rictor, Rptor independent companion of mTOR complex 2; MUT, mutated; UTR, untranslated region; NC, negative control.It has been reported that persistent or excessive autophagy promotes cancer cell death during chemotherapy, either by enhancing the induction of apoptosis or mediating autophagic cell death. Here, we show that miR-15a and miR-16 are potent inducers of autophagy. Rictor, a component of mTORC2 complex, is directly targeted by miR-15a/16. Overexpression of miR-15a/16 or depletion of endogenous Rictor attenuates the phosphorylation of mTORC1 and p70S6K, inhibits cell proliferation and G1/S cell cycle transition in human cervical carcinoma HeLa cells. Moreover, miR15a/16 dramatically enhances anticancer drug camptothecin (CPT)-induced autophagy and apoptotic cell death in HeLa cells. Collectively, these data demonstrate that miR-15a/16 induced autophagy contribute partly to their inhibition of cell proliferation and enhanced chemotherapeutic efficacy of CPT.

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“…Extracellular HMGB1 in its reduced form promotes autophagy through binding to the receptor for advanced glycation end products (RAGE) (19), which may contribute to lactate production and glutamine metabolism to sustain tumor growth (33). HMGB1-mediated autophagy increases chemoresistance in cancer cells such as colon cancer, pancreatic cancer, osteosarcoma, leukemia, gastric cancer, retinoblastoma and ovarian cancer (22,28,(34)(35)(36)(37)(38)(39)(40)(41). In addition, HMGB1-mediated autophagy in vitro or in vivo prevents polyglutamine aggregates in Huntington disease (42), systemic inflammation during sepsis (9,43), N-methyl-D-aspartate-induced excitotoxicity (44) and hepatic I/R injury (45,46) and sustains T-cell survival in myositis (47).…”

Section: Hmgb1 and Autophagymentioning

confidence: 99%