MiR-24 induces chemotherapy resistance and hypoxic advantage in breast cancer

Roscigno, Giuseppina; Puoti, Ilaria; Giordano, I.; Donnarumma, Elvira; Russo, Valentina; Affinito, Alessandra; Adamo, Assunta; Quintavalle, Cristina; Todaro, Matilde; Vivanco, María dM; Condorelli, Gerolama

doi:10.18632/oncotarget.14470

Cited by 67 publications

(46 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…miRNAs can either positively or negatively affect the development of tumors depending on their specific downstream target genes by base-pairing with their 3′-UTR. For example, miR-24 can induce chemotherapy resistance and hypoxic advantage in breast cancer through the downregulation of factor inhibiting HIF-1 ( 24 ). miR-497 is significantly correlated with temozolomide-resistance in glioma cells by regulating the insulin-like growth factor 1 receptor/insulin receptor substrate 1 pathway ( 25 ).…”

Section: Discussionmentioning

confidence: 99%

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

Yuan

Wei

Liu

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Tumorigenesis is a multistep process involving various cell growth-associated factors. Accumulated evidence indicates that the disordered regulation of microRNAs (miRNAs) contributes to tumorigenesis. However, the detailed mechanism underlying the involvement of miRNAs in oncogenesis remains to be fully elucidated. In the present study, the repressed expression of microRNA (miR)-494 was identified in 18 patients with osteosarcoma (OS) and OS cell lines, compared with corresponding controls. To determine whether deregulated miR-494 exerts tumor-suppressive effects in the development of OS, the effects of miR-494 on cell proliferation and metastasis were evaluated. It was found that the restoration of miR-494 in MG-63 and U2OS cells led to inhibited cell proliferation and attenuated migratory propensity in vitro, determined through analysis using MTT, colony formation and Transwell assays. In addition, overexpression of miR-494 markedly suppressed the tumor volume and weight in vivo. In accordance, the ectopic expression of miR-494 induced cell cycle arrest at the G1/S phase in OS cells. Bioinformatics analysis and luciferase reporter assays were performed to investigate the potential regulatory role of miR-494, the results of which indicated that miR-494 directly targeted cyclin-dependent kinase 6 (CDK6). Of note, the data obtained through reverse transcription-quantitative polymerase chain reaction and western blot analyses suggested that the elevated expression of miR-494 resulted in reduced mRNA and protein expression levels of CDK6. Taken together, these findings indicated that the miR-494/CDK6 axis has a significant tumor-suppressive effect on OS, and maybe a diagnostic and therapeutic target for the treatment of OS.

show abstract

Section: Discussionmentioning

confidence: 99%

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

Yuan

Wei

Liu

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…Several miRNAs have been found to be involved in the regulation of the stemness phenotype [4]. For instance, let-7 is one of the main regulators of self-renewal in breast cancer cells [5]; miR-127 and miR-128 have been shown to be important in the modulation of stemness in glioma, since their ablation enhances stem cell renewal and proliferation [6]; and, miR-24 was proven to be a powerful positive regulator of breast CSC features during hypoxic conditions [7]. Moreover, miR-216a-5p-encoded on chromosome 2 on the reverse strand and highly conserved across species-has been shown to act as a tumor suppressor in gastric cancer, breast cancer, hepatocellular carcinoma, small cell lung cancer and renal cancer [8][9][10][11].…”

mentioning

confidence: 99%

miR-216a Acts as a Negative Regulator of Breast Cancer by Modulating Stemness Properties and Tumor Microenvironment

Roscigno

Cirella

Affinito

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Breast cancer is the most frequent malignancy in females in terms of both incidence and mortality. Underlying the high mortality rate is the presence of cancer stem cells, which divide indefinitely and are resistant to conventional chemotherapies, so causing tumor relapse. In the present study, we identify miR-216a-5p as a downregulated microRNA in breast cancer stem cells vs. the differentiated counterpart. We demonstrate that overexpression of miR-216a-5p impairs stemness markers, mammosphere formation, ALDH activity, and the level of Toll-like receptor 4 (TLR4), which plays a significant role in breast cancer progression and metastasis by leading to the release of pro-inflammatory molecules, such as interleukin 6 (IL-6). Indeed, miR-216a regulates the crosstalk between cancer cells and the cells of the microenvironment, in particular cancer-associated fibroblasts (CAFs), through regulation of the TLR4/IL6 pathway. Thus, miR-216a has an important role in the regulation of stem phenotype, decreasing stem-like properties and affecting the cross-talk between cancer cells and the tumor microenvironment.

show abstract

“…Investigation of miRNA regulation in the kidney will improve the understanding of renal pathology and may eventually lead to the development of novel treatment strategies for reversing renal fibrosis and dysfunction. Results of previous studies revealed a critical role for miR-152 in human diseases, and miR-152 has been classified as an onco-miRNA in a variety of cancers, including breast, gastric and bladder cancers, and glioma (28)(29)(30). However, to date, a limited number of studies investigated the role of miR-152 in the urinary system.…”

Section: Discussionmentioning

confidence: 99%

miR‑152 regulates TGF‑β1‑induced epithelial‑mesenchymal transition by targeting HPIP in tubular epithelial cells

et al. 2018

View full text Add to dashboard Cite

Renal fibrosis is a common pathological feature of chronic kidney diseases, and their development and progression are influenced by epigenetic modifications including aberrant microRNA (miRNA or miR) expression. miRNAs have been demonstrated to modulate the aggressiveness of various cancers and have emerged as possible therapeutic agents for the management of renal fibrosis. Transforming growth factor β1 (TGF‑β1)‑induced epithelial‑mesenchymal transition (EMT) of tubular epithelial cells serves a role in the initiation and progression of renal fibrosis. Furthermore, recent results indicated that the progression of EMT is reversible. The present study aimed to clarify the role of miR‑152 in EMT of the tubular epithelial cell line HK‑2, stimulated by TGF‑β1, using in vitro transfection with a miR‑152 mimic and to further investigate the underlying mechanism of miR‑152 activity. In the present study, miR‑152 expression was significantly reduced in TGF‑β1‑treated HK‑2 cells, accompanied by an increased expression of hematopoietic pre‑B‑cell leukemia transcription factor (PBX)‑interacting protein (HPIP). Additionally, miR‑152 overexpression inhibited TGF‑β1‑induced EMT and suppressed HPIP expression by directly targeting the 3' untranslated region of HPIP in HK‑2 cells. Furthermore, upregulation of HPIP reversed miR‑152‑mediated inhibitory effects on the EMT. Collectively, the results suggest that downregulation of miR‑152 initiates the dedifferentiation of renal tubules and progression of renal fibrosis, which may provide important targets for prevention strategies of renal fibrosis.

show abstract

MiR-24 induces chemotherapy resistance and hypoxic advantage in breast cancer

Cited by 67 publications

References 71 publications

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

miR-216a Acts as a Negative Regulator of Breast Cancer by Modulating Stemness Properties and Tumor Microenvironment

miR‑152 regulates TGF‑β1‑induced epithelial‑mesenchymal transition by targeting HPIP in tubular epithelial cells

Contact Info

Product

Resources

About