HIF-1α Promotes Breast Cancer Cell MCF-7 Proliferation and Invasion Through Regulating miR-210

Zhang, Jiatong; Yan, Jinyin; Wang, Lu; Dai, Hao; Li, Ning; Hu, Wanning; Cai, Haifeng

doi:10.1089/cbr.2017.2270

Cited by 36 publications

(22 citation statements)

References 21 publications

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“…Also, the siHIF-1α overexpression significantly enhanced the HMGB3 silence induced decreased amounts of mammoshperes and increased levels of CD44 + CD24 − in the breast cancer cell, MDA-MB-231 cells. These findings suggest that siHIF-1α plays critical roles in the tumor growth or tumor cell proliferation and overexpression of siHIF-1α could obviously enhance tumor cell proliferation, which are consistent with the previous studies 45,46. Our results also proved that the HMGB3 interacted with HIF1α in MDA-MB-231 cells, which could explain the effects of HMGB3 on the tumor cell proliferation and mammosphere formation.…”

Section: Discussionsupporting

confidence: 93%

<p>HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1α</p>

Gu¹,

Xu²,

Huang³

et al. 2019

CMAR

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Background: Breast cancer is the most common malignant tumor that affects women with higher incidence. High-mobility group box 3 (HMGB3) plays critical functions in DNA repair, recombination, transcription and replication. This study aimed to investigate the effects of HMGB3 silence on mammosphere formation and tumor growth of breast cancer. Methods: LV5-HMGB3 and LV3-siHMGB3 vectors were transfected into MCF10A, MDA-MB-231, HCC1937, ZR-75-1 and MCF7 cells. Cell counting kit-8 (CCK-8) assay was used to evaluate cell proliferation. Xenograft tumor mice model was established by injection of MDA-MB-231. qRT-PCR and western blot were used to examine the expression of Nanog, Sox2 and OCT-4. Mammosphere forming assay was employed to evaluate mammosphere formation both in vivo and in vitro. Dual luciferase assay was utilized to verify the interaction between HMGB3 and hypoxia-inducible factor 1α (HIF1α). CD44 + /CD24 − was assessed with flow cytometry. Results: HMGB3 expression was higher significantly (p<0.05) in cancer cells compared to normal cells. HMGB3 overexpression significantly (p<0.05) enhanced and HMGB3 silence reduced cell proliferative mice compared to MCF10A and MDA-MB-231, respectively. HMGB3 overexpression enhanced and HMGB3 silence inhibited mammosphere formation. HMGB3 overexpression upregulated and HMGB3 silence downregulated Nanog, SOX2 and OCT-4 genes/proteins in MCF10A and MDA-MB-231 cells, respectively. HMGB3 silence reduced CD44 + /CD24 − levels in cancer cells. Silence of HMGB3 strengthened reductive effects of PTX on tumor sizes, iPSC biomarkers and mammosphere amounts in xenograft tumor mouse models. HMGB3 silence inhibited mammoshpere formation, cell proliferation and CD44 + CD24 − by interacting with HIF1α. Conclusion: HMGB3 silence could inhibit the cell proliferation in vitro and suppress tumor growth in vivo levels. The antitumor effects of HMGB3 silence were mediated by interacting with the HIF1α.

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Section: Discussionsupporting

confidence: 93%

<p>HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1α</p>

Gu¹,

Xu²,

Huang³

et al. 2019

CMAR

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“…Among all the miRNAs regulated by hypoxia through HIF-1α signaling, the most studied HRM is miR-210 [74][75][76]. Numerous studies aiming at the multifarious genes targeted by HIF-1α-induced miR-210 overexpression have highlighted the broad involvement of this mechanism in intricate cancer pathologies, including proliferation [33,45,46], apoptosis [34], angiogenesis [35], autophagy [36], metastasis [37][38][39], and radioresistance [40,47].…”

Section: Regulation Of Mir-210 Expression By Hif-1αmentioning

confidence: 99%

The interplay between HIF-1α and noncoding RNAs in cancer

Peng

Han

et al. 2020

J Exp Clin Cancer Res

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Hypoxia is a classic characteristic of the tumor microenvironment with a significant impact on cancer progression and therapeutic response. Hypoxia-inducible factor-1 alpha (HIF-1α), the most important transcriptional regulator in the response to hypoxia, has been demonstrated to significantly modulate hypoxic gene expression and signaling transduction networks. In past few decades, growing numbers of studies have revealed the importance of noncoding RNAs (ncRNAs) in hypoxic tumor regions. These hypoxia-responsive ncRNAs (HRNs) play pivotal roles in regulating hypoxic gene expression at the transcriptional, posttranscriptional, translational and posttranslational levels. In addition, as a significant gene expression regulator, ncRNAs exhibit promising roles in regulating HIF-1α expression at multiple levels. In this review, we briefly elucidate the reciprocal regulation between HIF-1α and ncRNAs, as well as their effect on cancer cell behaviors. We also try to summarize the complex feedback loop existing between these two components. Moreover, we evaluated the biomarker potential of HRNs for the diagnosis and prognosis of cancer, as well as the potential clinical utility of shared regulatory mechanisms between HIF-1α and ncRNAs in cancer treatment, providing novel insights into tumorigenicity, which may lead to innovative clinical applications.

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“…The expression of HIFs can promote the adaptation of tumor cells to hypoxia microenvironment [9]. Moreover, HIFs can further regulate a variety of genes related to invasion and metastasis of tumor cells [32,33]. The high expression of HIFs can be considered as a high risk factor of metastasis.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of the hypoxia-related DNA methylation-driven genes in lung adenocarcinoma progression

Hong

et al. 2020

Bioscience Reports

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Lung adenocarcinoma (LUAD) is a common type of lung cancer with high incidence and poor prognosis. Hypoxia and DNA methylation play important regulatory roles in cancer progression. The purpose of the present study was to explore the relationship between hypoxia and DNA methylation, and to identify key genes for hypoxia-regulated LUAD progression. Hypoxia score (HS) was calculated using the GSVA algorithm. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and protein–protein interaction (PPI) analysis were performed using clusterProfile package, STRING database and Cytoscape software. Kaplan–Meier curves of overall survival (OS) and disease-free survival (DFS) were drawn using R software. Smoking status and cancer stages were significantly associated with LUAD hypoxia, and hypoxia is a poor prognostic factor for LUAD. Compared with HS-low group, 1803 aberrantly methylated DEGs were identified in HS-high group. KEGG analysis showed that the 1803 genes were enriched in the metabolic pathways associated with hypoxia stress, angiogenesis and cancer progression. FAM20C, MYLIP and COL7A1 were identified as the hypoxia-related key genes in LUAD progression, which were regulated by DNA methylation. Hypoxia in LUAD tumor cells led to changes in DNA methylation patterns. In-depth study of the relationship between hypoxia and DNA methylation is helpful to elucidate the mechanism of tumorigenesis, and provides new ideas for LUAD treatment.

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HIF-1α Promotes Breast Cancer Cell MCF-7 Proliferation and Invasion Through Regulating miR-210

Abstract: MCF-7 cell proliferation was increased, invasion and migration were enhanced, with upregulated expression of HIF-1α mRNA and miR-210 in the hypoxic and anaerobic group following time extension.

Cited by 36 publications

References 21 publications

<p>HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1α</p>

<p>HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1α</p>

The interplay between HIF-1α and noncoding RNAs in cancer

Genome-wide analysis of the hypoxia-related DNA methylation-driven genes in lung adenocarcinoma progression

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