HMGB1 release promotes paclitaxel resistance in castration-resistant prostate cancer cells via activating c-Myc expression

Xiu, Lei; Hu, Xiaohong; Tin, Zhang; Zhang, Jian; Wu, Chuncheng; Hong, Wei; Jiang, Yinhui; Wang, Qinrong; Xie, Yuan; Zhao, Yan; Zhou, Jianjiang; Jin, Feng; Yu, Wenbin; Guo, Bin; Bai, Hua; Zhang, Qifang

doi:10.1016/j.cellsig.2020.109631

Cited by 26 publications

(13 citation statements)

References 33 publications

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“…Similar to STAT3, HMGB1 (high mobility group box 1) can regulate a wide variety of biological mechanisms such as differentiation, autophagy and migration [ 207 , 208 ]. HMGB1 overexpression promotes prostate cancer invasion via EMT induction [ 209 ]. Besides, HMGB1 can trigger chemoresistance feature of prostate cancer cells via activating downstream targets such as MYC/c-Myc signaling [ 209 ].…”

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

“…HMGB1 overexpression promotes prostate cancer invasion via EMT induction [ 209 ]. Besides, HMGB1 can trigger chemoresistance feature of prostate cancer cells via activating downstream targets such as MYC/c-Myc signaling [ 209 ]. The association between HMGB1 and autophagy is in favor of triggering gemcitabine resistance of prostate cancer cells.…”

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

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Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Ashrafizadeh

Paskeh

Mirzaei

et al. 2022

J Exp Clin Cancer Res

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Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a “self-degradation” mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients. Graphical abstract

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Section: Autophagy and Prostate Cancermentioning

confidence: 99%

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Ashrafizadeh

Paskeh

Mirzaei

et al. 2022

J Exp Clin Cancer Res

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“…A convincing body of evidence shows both increased expression of HMGB1 in several solid tumors and its critical role as an emerging prognostic factor in prostate cancer, breast cancer, and gastric cancer [122][123][124][125]. Biological responses downstream of HMGB1 are implicated in promoting tumor proliferation, migration, and invasion by stimulating production of pro-inflammatory cytokines through RAGE-dependent pathways [37]; however, HMGB1 can signal through TLRs (TLR2 and TLR4), as well as RAGE, thereby triggering NF-kB, STAT-3, and MyD88-dependent pathways and promoting inflammation and tumorigenesis [126][127][128].…”

Section: Inflammation In the Tmementioning

confidence: 99%

The RAGE/multiligand axis: a new actor in tumor biology

et al. 2022

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The receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein which actively participates in several chronic inflammation-related diseases. RAGE, in addition to AGEs, has a wide repertoire of ligands, including several damage-associated molecular pattern molecules or alarmins such as HMGB1 and members of the S100 family proteins. Over the last years, a large and compelling body of evidence has revealed the active participation of the RAGE axis in tumor biology based on its active involvement in several crucial mechanisms involved in tumor growth, immune evasion, dissemination, as well as by sculpturing of the tumor microenvironment as a tumor-supportive niche. In the present review, we will detail the consequences of the RAGE axis activation to fuel essential mechanisms to guarantee tumor growth and spreading.

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“…By providing acidic microenvironment for colorectal cancer cells, a decrease occurs in proliferation and drug sensitivity enhances due to transcriptional suppression of SOX2 (Ref. 292). Similarly, miRNAs are key players in TME and can dually inhibit/increase cancer progression via affecting TME and its components.…”

Section: Mirnas Sox2 and Tumour Microenvironmentmentioning

confidence: 99%

MicroRNAs regulating SOX2 in cancer progression and therapy response

Mirzaei

Saebfar²,

Gholami

et al. 2021

Expert Rev. Mol. Med.

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The proliferation, metastasis and therapy response of tumour cells are tightly regulated by interaction among various signalling networks. The microRNAs (miRNAs) can bind to 3′-UTR of mRNA and down-regulate expression of target gene. The miRNAs target various molecular pathways in regulating biological events such as apoptosis, differentiation, angiogenesis and migration. The aberrant expression of miRNAs occurs in cancers and they have both tumour-suppressor and tumour-promoting functions. On the contrary, SOX proteins are capable of binding to DNA and regulating gene expression. SOX2 is a well-known member of SOX family that its overexpression in different cancers to ensure progression and stemness. The present review focuses on modulatory impact of miRNAs on SOX2 in affecting growth, migration and therapy response of cancers. The lncRNAs and circRNAs can function as upstream mediators of miRNA/SOX2 axis in cancers. In addition, NF-κB, TNF-α and SOX17 are among other molecular pathways regulating miRNA/SOX2 axis in cancer. Noteworthy, anti-cancer compounds including bufalin and ovatodiolide are suggested to regulate miRNA/SOX2 axis in cancers. The translation of current findings to clinical course can pave the way to effective treatment of cancer patients and improve their prognosis.

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HMGB1 release promotes paclitaxel resistance in castration-resistant prostate cancer cells via activating c-Myc expression

Cited by 26 publications

References 33 publications

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

The RAGE/multiligand axis: a new actor in tumor biology

MicroRNAs regulating SOX2 in cancer progression and therapy response

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