MiR-323a-3p suppressed the glycolysis of osteosarcoma via targeting LDHA

Chen, Hanwen; Gao, Shuming; Cheng, Can

doi:10.1007/s13577-018-0215-0

Cited by 28 publications

(24 citation statements)

References 39 publications

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“…MicroRNA (miRNA), a kind of small non‐coding RNA, could inhibit translation or promote degradation of targets via combining to the specific region of 3′‐untranslated region (3′‐UTR) in targeted mRNA . Until now, several miRNAs like miR‐34a, miR‐34c, miR‐369‐3p, miR‐374a, miR‐30a‐5p, miR‐142‐3p, miR‐30d‐5p, miR‐323a‐3p, miR‑199a‑3p, miR‐449a, and miR‐4524a/b have been found to target the mRNA of LDHA . In a recent study on colorectal cancer, miR‐34a, miR‐34c, miR‐369‐3p, miR‐374a, and miR‐4524a/b were established to directly inhibit LDHA .…”

Section: Regulation Modes Of Ldhamentioning

confidence: 99%

Lactate dehydrogenase A: A key player in carcinogenesis and potential target in cancer therapy

et al. 2018

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Elevated glycolysis remains a universal and primary character of cancer metabolism, which deeply depends on dysregulated metabolic enzymes. Lactate dehydrogenase A (LDHA) facilitates glycolytic process by converting pyruvate to lactate. Numerous researches demonstrate LDHA has an aberrantly high expression in multiple cancers, which is associated with malignant progression. In this review, we summarized LDHA function in cancer research. First, we gave an introduction of structure, location, and basic function of LDHA. Following, we discussed the transcription and activation mode of LDHA. Further, we focused on the function of LDHA in cancer bio‐characteristics. Later, we discussed the clinical practice of LDHA in cancer prevention and treatment. What we discussed gives a precise insight into LDHA especially in cancer research, which will contribute to exploring cancer pathogenesis and its handling measures.

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Section: Regulation Modes Of Ldhamentioning

confidence: 99%

Lactate dehydrogenase A: A key player in carcinogenesis and potential target in cancer therapy

et al. 2018

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“…MiR-383 functioned as an inhibitor on the proliferation of ovarian cancer cell by targeting LDHA and suppressing the glycolysis [27]. A previous study showed that miR-323a-3p inhibited the growth of Osteosarcoma (OS) cell by targeting LDHA and suppressed the glycolysis of OS [28]. These results indicate that LDHA is a potential target of miRNAs to modulate the glucose metabolism of cancers.…”

Section: Discussionmentioning

confidence: 82%

“…Bioinformatics analysis results suggested that LDHA was a target of miR-638, and following luciferase reporter assay and RIP further confirmed the interaction. LDHA is a growth factor and has been proved to regulate cell proliferation and migration of VSMCs [22] Several publications have demonstrated that LDHA are regulated by the miRNAs [26][27][28]. Among these, LDHA promoted glycolysis and cell proliferation of breast cancer MCF-7 and MDA-MB-231 cells, and its beneficial effects on glycolysis and cell proliferation can be impaired by miR-34a [26].…”

Section: Discussionmentioning

confidence: 99%

MiR-638 repressed vascular smooth muscle cell glycolysis by targeting LDHA

Chen

et al. 2019

Open Medicine

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AbstractBackgroundAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) accelerated vascular diseases progression, like atherosclerosis and restenosis. MicroRNAs were reported to participate in modulating diverse cellular processes. Here, we focused on exploring the role of miR-638 in VSMCs glycolysis and underlying mechanism.MethodsCell Counting Kit-8 (CCK-8) assay was used to measure cell viability. Western blot assay was conducted to determine the expression of cell proliferation markers proliferating cell nuclear antigen (PCNA) and Ki-67, as well as Lactate dehydrogenase A (LDHA). VSMCs migration and invasion were evaluated by Transwell assay. Luciferase reporter gene assay and RNA immunoprecipitation were performed to validate the target relationship between miR-638 and LDHA. LDHA and miR-638 expression were also determined. Glycolysis of VSMCs was tested by corresponding Kits.ResultsPlatelet-derived growth factor-bb (PDGF-bb) promoted the VSMCs viability and down-regulated miR-638. Overexpression of miR-638 inhibited cell proliferation, migration and invasion of VSMCs. LDHA was identified as a target of miR-638, and counter-regulated by miR-638. Loss of miR-638 attenuated the suppressor effects on the proliferation, migration and invasion of VSMCs induced by LDHA down-regulation. MiR-638 inhibited the glycolysis of VSMCs by targeting LDHA.ConclusionMiR-638 is down-regulated by PDGF-bb treatment and suppressed the glycolysis of VSMCs via targeting LDHA.

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“…Similarly, also miR-323a-3p targets LDH-A and exerts a suppressive role of glycolysis and OS growth. In agreement, miR-323a-3p results significantly downregulated in OS tissues and cell lines, while its overexpression reduces cell viability [150]. In addition, a different miRNA, namely miR-186, which decreases indirectly lactate levels through direct inhibition of HIF-1α and glycolysis, functions as a tumor suppressor of both HOS and U2 OS cell lines, inhibiting tumor cell proliferation and invasion [151].…”

Section: Lactate and Sarcomasmentioning

confidence: 74%

Lactate in Sarcoma Microenvironment: Much More than just a Waste Product

Taddei

Pietrovito

Leo

et al. 2020

Cells

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Sarcomas are rare and heterogeneous malignant tumors relatively resistant to radio- and chemotherapy. Sarcoma progression is deeply dependent on environmental conditions that sustain both cancer growth and invasive abilities. Sarcoma microenvironment is composed of different stromal cell types and extracellular proteins. In this context, cancer cells may cooperate or compete with stromal cells for metabolic nutrients to sustain their survival and to adapt to environmental changes. The strict interplay between stromal and sarcoma cells deeply affects the extracellular metabolic milieu, thus altering the behavior of both cancer cells and other non-tumor cells, including immune cells. Cancer cells are typically dependent on glucose fermentation for growth and lactate is one of the most heavily increased metabolites in the tumor bulk. Currently, lactate is no longer considered a waste product of the Warburg metabolism, but novel signaling molecules able to regulate the behavior of tumor cells, tumor-stroma interactions and the immune response. In this review, we illustrate the role of lactate in the strong acidity microenvironment of sarcoma. Really, in the biological context of sarcoma, where novel targeted therapies are needed to improve patient outcomes in combination with current therapies or as an alternative treatment, lactate targeting could be a promising approach to future clinical trials.

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MiR-323a-3p suppressed the glycolysis of osteosarcoma via targeting LDHA

Cited by 28 publications

References 39 publications

Lactate dehydrogenase A: A key player in carcinogenesis and potential target in cancer therapy

Lactate dehydrogenase A: A key player in carcinogenesis and potential target in cancer therapy

MiR-638 repressed vascular smooth muscle cell glycolysis by targeting LDHA

Lactate in Sarcoma Microenvironment: Much More than just a Waste Product

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