miR‐505 acts as a tumor suppressor in gastric cancer progression through targeting HMGB1

Tian, Liang; Wang, Zheng-Yu; Hao, Jun; Zhang, Xiaoyu

doi:10.1002/jcb.28082

Cited by 28 publications

(21 citation statements)

References 34 publications

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“…Knockdown of HN1L led to a significant accumulation of DDX58, and a decrease of SMAD2, PIM1 and HMGB1 (Figure 5A). Recently, HMGB1 was reported to be over‐expressed in a number of cancers and involved in tumour invasion and metastasis 23‐27 . So we hypothesize that HN1L regulates the metastasis of breast cancer cell by HMGB1.…”

Section: Resultsmentioning

confidence: 82%

HN1L promotes migration and invasion of breast cancer by up‐regulating the expression of HMGB1

Jiao

Zhang

Chen

et al. 2020

J Cellular Molecular Medi

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The common sites for metastatic spread are bone, lung and liver. 3,4 Usually, the 5-year survival rate of advanced breast cancer is only 20%. 5 Metastasis and recurrence have become major obstacles to the survival of breast cancer patients. Therefore, screening and identification of the regulatory molecules closely related to the invasion and metastasis and exploring the molecular mechanisms are of great significance for the diagnosis and treatment of breast cancer. Haematological and neurological expressed 1-like (HN1L) belongs to the haematological and neurological expressed 1 (HN1) family. 6 The human HN1L gene, also known as L11, encodes a 190-aa protein. Previous reports showed that the expression of HN1 was up-regulated in prostate adenocarcinomas. 7,8 Moreover, HN1 could distinguish human ovarian carcinoma from healthy ovarian epithelial tissue. 9 Besides, HN1 negatively influenced the β-catenin/E-cadherin interaction, and contributed to migration in prostate cells. 10 HN1 also contributed to the migration, invasion and tumorigenesis of breast cancer by enhancing MYC activity. 11 However, not much is known

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Section: Resultsmentioning

confidence: 82%

HN1L promotes migration and invasion of breast cancer by up‐regulating the expression of HMGB1

Jiao

Zhang

Chen

et al. 2020

J Cellular Molecular Medi

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“…HMGB1 promotes GC cells proliferation and migration by activating the NF-кB and ERK signal pathways 11 , 12 . Although increasing evidence has shown that HMGB1 can induce the progression of GC 13 , the underlying molecular mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

Tang¹,

Wang²,

Cai

et al. 2021

J. Cancer

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Gastric cancer (GC) is a common malignancy tumour in China. Despite various therapeutic approaches to improve the survival rate of GC patients, the effectiveness of currently available treatments remains unsatisfactory. High mobility group box 1 (HMGB1) is reported to play a role in tumour development. However, the molecular mechanisms involved in HMGB1-mediated regulation of proliferation and migration of GC cells remain unclear. In the present study, we demonstrated that HMGB1 is highly expressed in GC cells and tissue. In HGC-27 GC cells, HMGB1 overexpression or HMGB1 RNA interference both demonstrated that HMGB1 could promote GC cell proliferation and migration. Investigation of the underlying molecular mechanisms revealed that HMGB1 enhanced cyclins expression, induced epithelial-to-mesenchymal transition and matrix metalloproteinase (MMPs) expression and promoted RAGE expression as well as RAGE-mediated activation of Akt/mTOR/P70S6K and ERK/P90RSK/CREB signalling pathways. We also found that inhibition of ERK and mTOR using specific inhibitors reduced recombinant human HMGB1-induced RAGE expression, suggesting that the RAGE-mTOR/ERK positive feedback loop is involved in HMGB1-induced GC cell proliferation and migration. Our study highlights a novel mechanism by which HMGB1 promotes GC cell proliferation and migration via RAGE-mediated Akt-mTOR and ERK-CREB signalling pathways which also involves the RAGE-mTOR/ERK feedback loop. These findings indicate that HMGB1 is a potential therapeutic target for GC.

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“…Additionally, HMGB1 was demonstrated to be a target gene of miR-1236-3p for the first time. In GC, HMGB1 has been verified to act as the target of miR-1179, 21 miR-129-5p 28 and miR-505 29 to modulate GC progression. In addition to a nuclear function as a DNA chaperone and cell death regulator, HMGB1 can be released into the extracellular environment to act as the prototypic damage-associated molecular pattern molecule.…”

Section: Discussionmentioning

confidence: 99%

<p>Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis</p>

Chen¹,

Chi²,

Xiang³

et al. 2020

CMAR

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Background: Circular RNAs (circRNAs) play an essential role in the pathogenesis of malignant tumors, including gastric cancer (GC). However, the effect of circ_0032821 on GC remains largely unknown. Methods: QRT-PCR assay was employed to examine the levels of circ_0032821, CEP128 mRNA and miR-1236-3p. RNase R digestion assay was utilized to verify the feature of circ_0032821. Cell Counting Kit-8 (CCK-8) assay and transwell assay were adopted to evaluate cell proliferation and metastasis. The level of glycolysis was evaluated through detecting ECAR, OCR, lactate production, glucose uptake and ATP synthesis. Dualluciferase reporter assay and RIP assay were conducted to analyze the relationship between miR-1236-3p and circ_0032821 or HMGB1. Western blot assay was adopted for high mobility group box 1 (HMGB1) level. Murine xenograft model assay was utilized for the effect of circ_0032821 in vivo. Results: High level of circ_0032821 was observed in GC tissues and cells. Silencing of circ_0032821 markedly repressed cell proliferation, metastasis and glycolysis in GC cells in vitro and blocked tumorigenesis of GC in vivo. For mechanism analysis, circ_0032821 was identified as the sponge of miR-1236-3p and HMGB1 was the target gene of miR-1236-3p. Moreover, miR-1236-3p suppression restored the influences of circ_0032821 deficiency on GC cell proliferation, metastasis and glycolysis. Overexpression of miR-1236-3p relieved the malignant behaviors of GC cells by targeting HMGB1. Conclusion: Circ_0032821 accelerated GC development through elevating HMGB1 expression via sponging miR-1236-3p.

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miR‐505 acts as a tumor suppressor in gastric cancer progression through targeting HMGB1

Cited by 28 publications

References 34 publications

HN1L promotes migration and invasion of breast cancer by up‐regulating the expression of HMGB1

HN1L promotes migration and invasion of breast cancer by up‐regulating the expression of HMGB1

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

<p>Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis</p>

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