MicroRNA‑34a directly targets high‑mobility group box 1 and inhibits the cancer cell proliferation, migration and invasion in cutaneous squamous cell carcinoma

Li, Shanshan; Luo, Chunxiong; Zhou, Jun; Zhang, Yong

doi:10.3892/etm.2017.5245

Cited by 17 publications

(14 citation statements)

References 28 publications

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“…A meta-analysis of 10 studies of non-small-cell lung cancer showed HMGB1 was increased in both serum and tissue of patients with cancer compared with samples from healthy lung samples (30). In models of bladder cancer (31), cutaneous squamous cell carcinoma (32), and gastric adenocarcinoma (33), inhibition of HMGB1 resulted in decreased cancer cell expansion. Overexpression of HMGB1 has been associated with increased resistance to chemotherapy, and suppression of HMGB1 results in increased chemosensitivity (34).…”

Section: Discussionmentioning

confidence: 99%

Targeting High Mobility Group Box-1 (HMGB1) Promotes Cell Death in Myelodysplastic Syndrome

Kam

Piryani

McCall

et al. 2019

Clinical Cancer Research

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Purpose: Myelodysplastic syndrome (MDS) is associated with a dysregulated innate immune system. The purpose of this study was to determine whether modulation of the innate immune system via high mobility group box-1 (HMGB1) could reduce cell viability in MDS.Experimental Design: We quantified HMGB1 in an MDS cell line MDS-L and in primary MDS cells compared with nonmalignant hematopoietic cells. We performed loss-offunction studies of HMGB1 using pooled siRNAs and a small-molecule inhibitor sivelestat compared with standard chemotherapy. We measured levels of engraftment of MDS-L cells in NOD-scidIL2Rg null (NSG) mice following treatment with sivelestat. Mechanistically, we interrogated cell survival pathways and 45 targets within the NFkB pathway using both protein analysis and a proteome profiler array.Results: We discovered that HMGB1 had increased expression in both MDS-L cells and in primary CD34 þ MDS cells compared with healthy CD34 þ hematopoietic cells. Sivelestat impaired MDS cell expansion, increased cellular death, and spared healthy hematopoietic cells. MDS-L marrow engraftment is reduced significantly at 17 weeks following treatment with sivelestat compared with control mice. Treatment of CD34 þ MDS cells with sivelestat and azacitidine or decitabine was additive to increase apoptotic cell death compared with chemotherapy alone. Sivelestat promoted apoptosis with increased expression of PUMA, activated caspase 3, and increased DNA double-strand breaks. Inhibition of HMGB1 reduced levels of Toll-like receptors (TLR) and suppressed activation of NFkB in MDS-L cells.Conclusions: Inhibition of HMGB1 could promote MDS cell death and alter innate immune responses via suppression of NFkB pathways.

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Section: Discussionmentioning

confidence: 99%

Targeting High Mobility Group Box-1 (HMGB1) Promotes Cell Death in Myelodysplastic Syndrome

Kam

Piryani

McCall

et al. 2019

Clinical Cancer Research

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Section: Non-coding Rna Modifications In Cutaneous Sccmentioning

confidence: 99%

“…The underexpression of miR-34a is associated with the aggressive progression of cSCC [ 79 , 80 ]. Studies suggest that miR-34a is a tumor suppressor whose restoration inhibits proliferation, migration and invasion of cancer cells by modulating the expression of HMGB1 and SIRT6 [ 80 ]. The first target is a nuclear-binding protein that participates in the regulation of DNA organization and gene transcription, while the second targeted gene is a NAD+-dependent histone deacetylase and ADP ribosyl transferase that has been implicated in DNA repair, genomic stability and telomere structure [ 81 ].…”

Section: Non-coding Rna Modifications In Cutaneous Sccmentioning

confidence: 99%

Deciphering the Molecular Landscape of Cutaneous Squamous Cell Carcinoma for Better Diagnosis and Treatment

Lazăr

Dinescu

Costache

2020

JCM

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Cutaneous squamous cell carcinoma (cSCC) is a common type of neoplasia, representing a terrible burden on patients’ life and clinical management. Although it seldom metastasizes, and most cases can be effectively treated with surgical intervention, once metastatic cSCC displays considerable aggressiveness leading to the death of affected individuals. No consensus has been reached as to which features better characterize the aggressive behavior of cSCC, an achievement hindered by the high mutational burden caused by chronic ultraviolet light exposure. Even though some subtypes have been recognized as high risk variants, depending on certain tumor features, cSCC that are normally thought of as low risk could pose an increased danger to the patients. In light of this, specific genetic and epigenetic markers for cutaneous SCC, which could serve as reliable diagnostic markers and possible targets for novel treatment development, have been searched for. This review aims to give an overview of the mutational landscape of cSCC, pointing out established biomarkers, as well as novel candidates, and future possible molecular therapies for cSCC.

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“…For instance, miR-199a/b-3p suppresses the proliferation of gastric cancer cells by regulating P21 activated kinase 4/mitogen activated protein kinase/extracellular signal-regulated kinase signaling pathway (11). Li et al (12) indicated that miR-34a directly targeted high-mobility group box 1 and inhibited the proliferation, migration and invasion of cancer cells in cutaneous squamous cell carcinoma. In EC, Zhao et al (13) revealed that miR-126 inhibited the migration and invasion of EC cells by targeting insulin receptor substrate 1.…”

Section: Introductionmentioning

confidence: 99%

miR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway

Zhu

Wang²,

Wang

et al. 2018

Mol Med Report

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MicroRNAs (miRs) are essential regulators in the development and progression of cancer. The role of miR-494-3p in endometrial cancer (EC) has not yet been investigated. In the present study, the expression levels of miR-494-3p were significantly upregulated in EC tissues compared with adjacent normal tissues. Furthermore, upregulation of miR-494-3p in patients with EC indicated poorer prognosis; miR-494-3p overexpression significantly promoted the proliferation, migration and invasion of HHUA and JEC cells in vitro. Consistently, inhibition of miR-494-3p in HHUA cells significantly suppressed tumor growth in vivo in a xenograft model. Additionally, phosphatase and tensin homolog (PTEN) was revealed to be a direct target of miR-494-3p in EC cells. Furthermore, overexpression of miR-494-3p inhibited PTEN expression and consequently activated the downstream phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signialing pathway. Restoration of PTEN or inhibition of PI3K/AKT pathway also abolished miR-494-3p-mediated proliferation, migration and invasion of HHUA and JEC cells. In summary, the results of the present study revealed the importance of the miR-494-3p/PTEN/PI3K/AKT axis in the progression of EC, which may provide novel insight into potential therapeutic targets for the treatment of EC.

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MicroRNA‑34a directly targets high‑mobility group box 1 and inhibits the cancer cell proliferation, migration and invasion in cutaneous squamous cell carcinoma

Cited by 17 publications

References 28 publications

Targeting High Mobility Group Box-1 (HMGB1) Promotes Cell Death in Myelodysplastic Syndrome

Targeting High Mobility Group Box-1 (HMGB1) Promotes Cell Death in Myelodysplastic Syndrome

Deciphering the Molecular Landscape of Cutaneous Squamous Cell Carcinoma for Better Diagnosis and Treatment

miR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway

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