microRNA-877-5p exerts tumor-suppressive functions in prostate cancer through repressing transcription of forkhead box M1

Yang, Bin; Diao, Huifeng; Wang, Pu; Guan, Fengju; Liu, Hechen

doi:10.1080/21655979.2021.1989969

Cited by 15 publications

(11 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have reported that the dysregulation of miRNA expression profiles is associated with PC and emerged as a novel biomarker and potential therapeutic target for the treatment of PC ( 33 , 36 , 37 ). According to the report, miR-877-5p may act as a suppressor in PC and reduces cancer cell proliferation, migration and invasion by targeting FOXM1 ( 38 ). miRNA-125b has been attributed as an oncogene in the pathogenesis of PC through down regulation of Bak1 ( 39 ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel

Xia¹,

Wang²,

Qi³

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

The expression of O-GlcNAc transferase (OGT) and its catalytic product, O-GlcNAcylation (O-GlcNAc), are elevated in many types of cancers, including prostate cancer (PC). Inhibition of OGT serves as a potential strategy for PC treatment alone or combinational therapy. PC is the second common cancer type in male worldwide, for which chemotherapy is still the first-line treatment. However, the function of inhibition of OGT on chemotherapeutic response in PC cells is still unknown. In this study, we show that inhibition of OGT by genetic knockdown using shRNA or by chemical inhibition using OGT inhibitors sensitize PC cells to docetaxel, which is the most common chemotherapeutic agent in PC chemotherapy. Furthermore, we identified that microRNA-140 (miR-140) directly binds to OGT mRNA 3′ untranslated region and inhibits OGT expression. Moreover, docetaxel treatment stimulates miR-140 expression, whereas represses OGT expression in PC cells. Overexpression of miR-140 enhanced the drug sensitivity of PC cells to docetaxel, which could be reversed by overexpression of OGT. Overall, this study demonstrates miR-140/OGT axis as therapeutic target in PC treatment and provides a promising adjuvant therapeutic strategy for PC therapy.

show abstract

Section: Introductionmentioning

confidence: 99%

Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel

Xia¹,

Wang²,

Qi³

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…Luo et al uncovered that miR-877-5p restrains PDAC progression via negatively regulating lncRNA NR2F1-AS1 [ 45 ]. Additionally, researchers have confirmed miR-877-5p as a positive element in other malignancies [ 46 , 47 ]. Herein, we firstly reported the involvement of miR-877-5p in CML.…”

Section: Discussionmentioning

confidence: 99%

circCRKL, a circRNA derived from CRKL, regulates BCR-ABL via sponging miR-877-5p to promote chronic myeloid leukemia cell proliferation

et al. 2022

View full text Add to dashboard Cite

Background The BCR-ABL fusion protein is the key factor that results in the occurrence of chronic myeloid leukemia (CML). Imatinib (IM) is a targeted inhibitor of BCR-ABL to achieve complete remission. However, remission failure occurs due to acquired resistance caused by secondary BCR-ABL mutations, underlining the need for novel BCR-ABL-targeting strategies. Circular RNAs (circRNAs) derived from tumor-related genes have been revealed as possible therapeutic targets for relevant cancers in recent investigations. In CML, the roles of this kind of circRNA are yet obscure. Methods Firstly, RT-qPCR was used for determining circCRKL expression level in cell lines and clinical samples, RNase R and Actinomycin D were employed to verify the stability of circCRKL. Then shRNAs were designed to specifically knockdown circCRKL. The function of circCRKL in vitro was investigated using CCK-8, colony formation assay, and flow cytometry, while a CML mouse model was constructed to explore the function in vivo. Finally, a dual-luciferase reporter assay, RNA pull-down, RNA immunoprecipitation, and rescue experiments were conducted to investigate the mechanism of circCRKL functioning. Results Here, we determined circCRKL, which derives from CML-relevant gene CRKL, is over-expressed in BCR-ABL+ cells. Then we noticed knocking down circCRKL using shRNA lentivirus dampens the proliferation of BCR-ABL+ cells both in vitro and in vivo, and augments susceptibility of resistant cells to IM. Intriguingly, we observed that circCRKL has a considerable impact on the expression level of BCR-ABL. Mechanistically, circCRKL could behave like a decoy for miR-877-5p to enhance the BCR-ABL level, allowing BCR-ABL+ cells to maintain viability. Conclusions Overall, the current study uncovers that circCRKL is specifically expressed and regulates BCR-ABL expression level via decoying miR-877-5p in BCR-ABL+ cells, highlighting that targeting circCRKL along with imatinib treatment could be utilized as a potential therapeutic strategy for CML patients.

show abstract

“…The cell proliferation capacity of PCa cells transfected with Oe-TMEM100 or co-transfected with sh-GATA5 was measured using a CCK-8 assay [ 21 ]. Briefly, transfected DU145 cells were seeded into 96-well plates at a density of 5 × 10 3 cells/well.…”

Section: Methodsmentioning

confidence: 99%

GATA binding protein 5-mediated transcriptional activation of transmembrane protein 100 suppresses cell proliferation, migration and epithelial-to-mesenchymal transition in prostate cancer DU145 cells

et al. 2022

View full text Add to dashboard Cite

It has been reported that transmembrane protein 100 (TMEM100) acts as a tumor regulator in several types of cancers. However, whether the expression of TMEM100 is associated with the development and prognosis of prostate cancer (PCa) remains elusive. Therefore, the present study aimed to uncover the role of GATA binding protein 5 (GATA5)-mediated activation of TMEM100 in the proliferation, migration and epithelial-to-mesenchymal transition (EMT) of PCa cells. The expressions of TMEM100 and GATA5 in PCa patients were analyzed by the GEPIA database. The binding site of GATA5 and TMEM100 promoter was predicted by the JASPAR database. Expressions of TMEM100 and GATA5 in PCa cells were detected by qRT-PCR and Western blot analysis. Cell Counting Kit 8 and colony formation assays were performed to measure cell proliferation. In addition, cell migration, invasion and the expression of EMT-associated proteins were evaluated using wound healing, transwell assay and Western blotting assays, respectively. The bioinformatics analysis revealed that TMEM100 was downregulated in PCa and was associated with overall survival of PCa. In addition, TMEM10 overexpression attenuated cell proliferation, migration, invasion and EMT in PCa cells. The interaction between TMEM100 and GATA5 was verified using dual luciferase reporter and chromatin immunoprecipitation assays. Furthermore, the results showed that GATA5 was downregulated and GATA5 silencing reversed the inhibitory effects of TMEM10 on PCa cells. Overall, the current study suggested that the GATA5-mediated transcriptional activation of TMEM100 could affect the behavior of PCa cells and was associated with poor prognosis in PCa.

show abstract

microRNA-877-5p exerts tumor-suppressive functions in prostate cancer through repressing transcription of forkhead box M1

Cited by 15 publications

References 38 publications

Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel

Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel

circCRKL, a circRNA derived from CRKL, regulates BCR-ABL via sponging miR-877-5p to promote chronic myeloid leukemia cell proliferation

GATA binding protein 5-mediated transcriptional activation of transmembrane protein 100 suppresses cell proliferation, migration and epithelial-to-mesenchymal transition in prostate cancer DU145 cells

Contact Info

Product

Resources

About