miR‐548c‐5p inhibits colorectal cancer cell proliferation by targeting PGK1

Ge, Jianxin; Li, Jun; Su, Naichuan; Wang, Pingping; Zhao, Guifeng; Zhang, Xiaoyan

doi:10.1002/jcp.28525

Cited by 36 publications

(19 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because of this, scientists are working hard to explore PGK1 inhibitors. Very recently, miRNA-450b-3p, miR-548c-5p, miRNA-215-5p, and miR-6869-5p have been reported to directly target PGK1 3 -UTR and repress PGK1 expression (Chen et al, 2019(Chen et al, , 2020Ge et al, 2019;Wang et al, 2020). However, it remains unknown whether these miRNAs regulate the Warburg effect and whether the Warburg effect is responsible for cancer cell growth by these miRNAs.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have shown that miRNAs are involved in cancer cell proliferation, invasion and metastasis. Recently, miRNA-450b-3p, miRNA-548c-5p, miRNA-215-5p, and miRNA-6869-5p have been shown to directly target PGK1 3 -UTR and inhibit PGK1 expression (Chen et al, 2019(Chen et al, , 2020Ge et al, 2019;Wang et al, 2020). These miRNAs can regulate cancer cell proliferation, migration and/or invasion.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Liang²,

Zhang³

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

The Warburg effect (aerobic glycolysis) is a hallmark of cancer and is becoming a promising target for diagnosis and therapy. Phosphoglycerate kinase 1 (PGK1) is the first adenosine triphosphate (ATP)-generating glycolytic enzyme in the aerobic glycolysis pathway and plays an important role in cancer development and progression. However, how microRNAs (miRNAs) regulate PGK1-mediated aerobic glycolysis remains unknown. Here, we show that miR-16-1-3p inhibits PGK1 expression by directly targeting its 3′-untranslated region. Through inhibition of PGK1, miR-16-1-3p suppressed aerobic glycolysis by decreasing glucose uptake, lactate and ATP production, and extracellular acidification rate, and increasing oxygen consumption rate in breast cancer cells. Aerobic glycolysis regulated by the miR-16-1-3p/PGK1 axis is critical for modulating breast cancer cell proliferation, migration, invasion and metastasis in vitro and in vivo. In breast cancer patients, miR-16-1-3p expression is negatively correlated with PGK1 expression and breast cancer lung metastasis. Our findings provide clues regarding the role of miR-16-1-3p as a tumor suppressor in breast cancer through PGK1 suppression. Targeting PGK1 through miR-16-1-3p could be a promising strategy for breast cancer therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Liang²,

Zhang³

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…For example, bone marrow MSC‒derived miR‐1180 accelerates ovarian cancer cell growth and glycolysis through the SFRP1/Wnt pathway 48 . MiR‐548c‐5p represses cell proliferation via targeting PGK1 in colorectal cancer 49 . Accumulating evidence has demonstrated that lncRNAs can function as ceRNAs by competitively binding to miRNAs in various cancers 50,51 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA MAGI2‐AS3/miR‐218‐5p/GDPD5/SEC61A1 axis drives cellular proliferation and migration and confers cisplatin resistance in nasopharyngeal carcinoma

Cao

Zhou

2020

Int Forum Allergy Rhinol

View full text Add to dashboard Cite

Background: Nasopharyngeal carcinoma (NPC), a subclass of neck and head cancers, is the predominant cause of cancer-associated death globally. LncRNA MAGI2-AS3 has been previously reported to be associated with multiple cancers, but its molecular mechanism in NPC has not been fully explained. Hence, the purpose of this study is to identify the role and regulatory mechanism of MAGI2-AS3 in NPC. Methods: Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB) were employed to examine gene levels. The biologic function of MAGI2-AS3 in NPC was estimated by cell counting, EdU, Transwell, and WB assays. Luciferase reporter and radioimmunoprecipitation (RIP) assays were carried out to determine the combination between miR-218-5p and MAGI2-AS3, GDPD5, and SEC61A1. Results: MAGI2-AS3 is expressed at a high level in NPC cell lines. Moreover, MAGI2-AS3 knockdown-suppressed NPC progression in vitro and in vivo. Furthermore, MAGI2-AS3 functioned as a competing endogenous RNA (ceRNA) by sponging miR-218-5p to increase the expression of GDPD5 in NPC. Importantly, it was found that MAGI2-AS3 regulated NPC progression and cisplatin resistance via modulating GDPD5. In addition, MAGI2-AS3 could also promote the proliferation and migration in NPC cells by regulating SEC61A1. Conclusion: MAGI2-AS3/miR-218-5p/GDPD5/SEC61A1 axis drove cell proliferation, migration, and epithelialmesenchymal transition, and conferred cisplatin resistance in NPC, which may provide a novel insight into the development of NPC.

show abstract

“…In addition to upregulated miRNAs, downregulated miRNAs such as miR-144 , miR-548c-5p , and miR-198 also play important roles in tumorigenesis. MiR-144 has been reported to target GSPT1 to inhibit the metastasis of CRC (Xiao et al, 2015), and miR-548c-5p has been found to act as a tumor suppressor in CRC by targeting PGK1 (Ge et al, 2019). The above results indicate that dysregulated miRNA expression has been observed in CRC and that the abnormal expression of specific miRNAs is associated with metastasis and prognosis in CRC.…”

Section: Discussionmentioning

confidence: 99%

MiR-506 Targets UHRF1 to Inhibit Colorectal Cancer Proliferation and Invasion via the KISS1/PI3K/NF-κB Signaling Axis

Lin

Chen

Zheng

et al. 2019

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

BackgroundThe UHRF1 gene is an epigenetic modification factor that mediates tumor suppressor gene silencing in a variety of cancers. Related studies have reported that UHRF1 can inhibit the expression of the KISS1 gene. However, the regulatory mechanism underlying UHRF1 expression in colorectal cancer (CRC) is still unclear. The aim of this study was to gain a better understanding of the regulation of UHRF1 expression in CRC and to determine whether it regulates the mechanism by which KISS1 promotes CRC metastasis.MethodsIn the present study, the levels of miR-506, UHRF1 and KISS1 expression in CRC tissues and in human CRC cell lines were studied using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation, migration, and invasion assays are used to detect cell proliferation, migration, and invasion. A dual-luciferase reporter system was used to confirm the target gene of miR-506.ResultsThis study found that UHRF1 protein is highly expressed in CRC tissues and negatively correlated with KISS1 protein expression. UHRF1 overexpression activates the PI3K/NF-κB signaling pathway by inhibiting the mRNA expression levels of pathway mediators. Bioinformatics analysis and luciferase reporter gene assays confirmed that miR-506 targets UHRF1.ConclusionThis study identified the regulation of UHRF1 expression in CRC and the mechanism of CRC metastasis. UHRF1 may be a new potential target molecule for future CRC metastasis treatment.

show abstract

miR‐548c‐5p inhibits colorectal cancer cell proliferation by targeting PGK1

Cited by 36 publications

References 39 publications

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Long noncoding RNA MAGI2‐AS3/miR‐218‐5p/GDPD5/SEC61A1 axis drives cellular proliferation and migration and confers cisplatin resistance in nasopharyngeal carcinoma

MiR-506 Targets UHRF1 to Inhibit Colorectal Cancer Proliferation and Invasion via the KISS1/PI3K/NF-κB Signaling Axis

Contact Info

Product

Resources

About