Silencing of let-7b-5p inhibits ovarian cancer cell proliferation and stemness characteristics by Asp-Glu-Ala-Asp-box helicase 19A

Huang, Xiujuan; Hua, Dong; Liu, Yang; Yu, Fang; Yang, Shi Yu; Chen, Zhen; Li, Jueying

doi:10.1080/21655979.2021.1982276

Cited by 3 publications

(2 citation statements)

References 46 publications

(46 reference statements)

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“…Furthermore, dual-luciferase report assays and qRT-PCR confirmed the direct combination and regulation of hsa-let-7b-5p onSLC35A2. In several malignancies, hsa-let-7b-5p assumes the role of a tumor suppressor, such as esophageal squamous cell carcinoma [39], multiple myeloma [40], AML [41] and ovarian serous cystadenocarcinoma [42]. In BRCA, a miRNA panel including hsa-let-7b-5p in peripheral blood was demonstrated to be potential signatures for breast cancer diagnosis [43,44].…”

Section: Discussionmentioning

confidence: 99%

SLC35A2 expression drives breast cancer progression via ERK pathway activation

Yang,

Tao,

et al. 2024

The FEBS Journal

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Alterations in glycosylation are associated with breast tumor formation and progression. Nevertheless, the specific functions and mechanisms of the human major UDP‐galactose transporter‐encoding gene Solute carrier family 35 member A2 (SLC35A2) in breast invasive carcinoma (BRCA) have not been fully determined. Here we reportthat SLC35A2promotesBRCA progression via activating ERK. SLC35A2 expression and prognosis‐predictive significance in pan‐cancer were evaluated using publicdatabases. The upstream non‐coding RNAs (ncRNAs) of SLC35A2 were analyzed, and their expressions and regulations were validated in breast tissues and cell lines by quantitative polymerase chain reaction (qPCR) and dual‐luciferase assays. We used bioinformatic tools to assess the link between SLC35A2 expression and immune infiltration, and performed immunohistochemistry for validation. CCK8, EdU, transwell, flow cytometer, and westernblottingwere used to assess the proliferation, motility, cell cycleand apoptosis of BRCA cells in vitro. The xenograft models were constructed to assess the effect of SLC35A2 on BRCA tumor growth in vivo. The results indicated thatSLC35A2 expression was upregulated and linked to an unfavorable prognosis in BRCA. The most likely upstream ncRNA‐associated pathway of SLC35A2 in BRCA was the AC074117.1/hsa‐let‐7b‐5p axis. SLC35A2 expression had positive correlations with the presence of Th2 cells, regulatory T cells, and immune checkpoints. Knockdown ofSLC35A2could reduce BRCA cell proliferation, motility, and cause G2/M arrest and cell apoptosis via ERK signaling. Moreover, ERK activation can rescue the inhibitory effects of knockdownSLC35A2in BRCA. In conclusion, AC074117.1/hsa‐let‐7b‐5p axis‐mediated high expression of SLC35A2 acts as a tumor promoter in BRCA via ERK signaling, which provides a potential target for BRCA treatment.

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Section: Discussionmentioning

confidence: 99%

SLC35A2 expression drives breast cancer progression via ERK pathway activation

Yang,

Tao,

et al. 2024

The FEBS Journal

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“…The anti-cancer roles were also confirmed in other cancers, such as human glioma and gastric cancer [ 36 , 37 ]. As a tumor-promoting factor, let-7b-5p is overexpressed in ovarian cancer, and its silence dampens ovarian cancer cell proliferation [ 38 ]. Suppression of let-7b-5p is conducive to an anti-tumorigenic macrophage phenotype in prostate cancer by SOCS1/STAT pathway [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Let-7b-5p inhibits breast cancer cell growth and metastasis via repression of hexokinase 2-mediated aerobic glycolysis

Li¹,

Zhang²,

Lin

et al. 2023

Cell Death Discov.

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Hexokinase 2 (HK2), a critical rate-limiting enzyme in the glycolytic pathway catalyzing hexose phosphorylation, is overexpressed in multiple human cancers and associated with poor clinicopathological features. Drugs targeting aerobic glycolysis regulators, including HK2, are in development. However, the physiological significance of HK2 inhibitors and mechanisms of HK2 inhibition in cancer cells remain largely unclear. Herein, we show that microRNA-let-7b-5p (let-7b-5p) represses HK2 expression by targeting its 3′-untranslated region. By suppressing HK2-mediated aerobic glycolysis, let-7b-5p restrains breast tumor growth and metastasis both in vitro and in vivo. In patients with breast cancer, let-7b-5p expression is significantly downregulated and is negatively correlated with HK2 expression. Our findings indicate that the let-7b-5p/HK2 axis plays a key role in aerobic glycolysis as well as breast tumor proliferation and metastasis, and targeting this axis is a potential therapeutic strategy for breast cancer.

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The Metabolism Reprogramming of microRNA Let-7-Mediated Glycolysis Contributes to Autophagy and Tumor Progression

Liao

2021

IJMS

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Cancer is usually a result of abnormal glucose uptake and imbalanced nutrient metabolization. The dysregulation of glucose metabolism, which controls the processes of glycolysis, gives rise to various physiological defects. Autophagy is one of the metabolic-related cellular functions and involves not only energy regeneration but also tumorigenesis. The dysregulation of autophagy impacts on the imbalance of metabolic homeostasis and leads to a variety of disorders. In particular, the microRNA (miRNA) Let-7 has been identified as related to glycolysis procedures such as tissue repair, stem cell-derived cardiomyocytes, and tumoral metastasis. In many cancers, the expression of glycolysis-related enzymes is correlated with Let-7, in which multiple enzymes are related to the regulation of the autophagy process. However, much recent research has not comprehensively investigated how Let-7 participates in glycolytic reprogramming or its links to autophagic regulations, mainly in tumor progression. Through an integrated literature review and omics-related profiling correlation, this review provides the possible linkage of the Let-7 network between glycolysis and autophagy, and its role in tumor progression.

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Silencing of let-7b-5p inhibits ovarian cancer cell proliferation and stemness characteristics by Asp-Glu-Ala-Asp-box helicase 19A

Cited by 3 publications

References 46 publications

SLC35A2 expression drives breast cancer progression via ERK pathway activation

SLC35A2 expression drives breast cancer progression via ERK pathway activation

Let-7b-5p inhibits breast cancer cell growth and metastasis via repression of hexokinase 2-mediated aerobic glycolysis

The Metabolism Reprogramming of microRNA Let-7-Mediated Glycolysis Contributes to Autophagy and Tumor Progression

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