Targeting miR-21-3p inhibits proliferation and invasion of ovarian cancer cells

Báez-Vega, Perla M.; Vargas, Ileabett M. Echevarría; Valiyeva, Fatma; Encarnación-Rosado, Joel; Román, A.; Flores, Josean; Marcos-Martínez, María J.; Vivas‐Mejía, Pablo E.

doi:10.18632/oncotarget.9216

Cited by 93 publications

(77 citation statements)

References 35 publications

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“…ZNF608 is associated with transcriptional events [221]. By inhibiting those three downstream targets, miR-21-3p contributes to tumorigenesis and CSC proliferation [222]. In the cervical cancer cell lines Hela, CaSki, Siha, and C33A, miR-23b decreases the tumorsphere amount and size, suppresses stem marker expression, and decreases cell resistance to cisplastin via inhibition of the expression of aldehyde dehydrogenase 1 family member A1 (ALDHA1) [223].…”

Section: Discussionmentioning

confidence: 99%

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Jiao

Qian

et al. 2019

Cells

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Cancer ranks as the second leading cause of death worldwide, causing a large social and economic burden. However, most anti-cancer treatments face the problems of tumor recurrence and metastasis. Therefore, finding an effective cure for cancer needs to be solved urgently. Recently, the discovery of cancer stem cells (CSCs) provides a new orientation for cancer research and therapy. CSCs share main characteristics with stem cells and are able to generate an entire tumor. Besides, CSCs usually escape from current anti-cancer therapies, which is partly responsible for tumor recurrence and poor prognosis. microRNAs (miRNAs) belong to small noncoding RNA and regulate gene post-transcriptional expression. The dysregulation of miRNAs leads to plenty of diseases, including cancer. The aberrant miRNA expression in CSCs enhances stemness maintenance. In this review, we summarize the role of miRNAs on CSCs in the eight most common cancers, hoping to bridge the research of miRNAs and CSCs with clinical applications. We found that miRNAs can act as tumor promoter or suppressor. The dysregulation of miRNAs enhances cell stemness and contributes to tumor metastasis and therapeutic resistance via the formation of feedback loops and constitutive activation of carcinogenic signaling pathways. More importantly, some miRNAs may be potential targets for diagnosis, prognosis, and cancer treatments.

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Section: Discussionmentioning

confidence: 99%

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Jiao

Qian

et al. 2019

Cells

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“…The miR-17-92 cluster, an oncomiR, presents a high frequency of genomic alterations [123] and it induces angiogenesis through inhibition of thrombospondin 1 [124]. miR-21, an oncomir, regulates Phosphatase and tensin homolog (PTEN), this enzyme acts as a tumor suppressor [125], it has an inverse relation with programmed cell death protein 4 (PDCD4) expression [126] and it exerts an inhibitory effect on cancer cell proliferation [127]. This miR has also been associated with recurrence-free survival, which will be lower if miR-21 levels are elevated [128].…”

Section: Role Of Mirs In Ovarian Cancermentioning

confidence: 99%

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Retamales-Ortega

Oróstica

Vera

et al. 2017

IJMS

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Ovarian cancer is the eighth most common cancer in women worldwide, and epithelial ovarian cancer (EOC) represents 90% of cases. Nerve growth factor (NGF) and its high affinity receptor tyrosine kinase A receptor (TRKA) have been associated with the development of several types of cancer, including EOC; both NGF and TRKA levels are elevated in this pathology. EOC presents high angiogenesis and several molecules have been reported to induce this process. NGF increases angiogenesis through its TRKA receptor on endothelial cells, and by indirectly inducing vascular endothelial growth factor expression. Other molecules controlled by NGF include ciclooxigenase-2, disintegrin and metalloproteinase domain-containing protein 17 (ADAM17) and calreticulin (CRT), proteins involved in crucial processes needed for EOC progression. These molecules could be modified through microRNA regulation, which could be regulated by NGF. MicroRNAs are the widest family of non-coding RNAs; they bind to 3′-UTR of mRNAs to inhibit their translation, to deadenilate or to degraded them. In EOC, a deregulation in microRNA expression has been described, including alterations of miR-200 family, cluster-17-92, and miR-23b, among others. Since the NGF-microRNA relationship in pathologies has not been studied, this review proposes that some microRNAs could be associated with NGF/TRKA activation, modifying protein levels needed for EOC progression.

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“…Previous studies reported that the overexpression of miR‐21 is associated with the invasion and metastasis of various human cancer cells . Therefore, in order to determine whether miR‐21‐3p was necessary for cell invasion and migration, transwell assay and wound healing assay were performed to detect the invasive as well as migratory abilities of the HCT116 cells, respectively, following transfection with miR‐21‐3p inhibitors or NC‐miRNA.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of microRNA‐21‐3p suppresses proliferation as well as invasion and induces apoptosis by targeting RNA‐binding protein with multiple splicing through Smad4/extra cellular signal‐regulated protein kinase signalling pathway in human colorectal cancer HCT116 cells

Hou

Guo

Zhao

et al. 2018

Clin Exp Pharma Physio

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MicroRNA-21-3p (miR-21-3p), the passenger strand of pre-mir-21, has been found to be high-expressing in various cancers and to be associated with tumour malignancy, which is proposed as a novel focus in malignant tumours. Colorectal cancer (CRC), currently known as one of the most prevalent malignancy, is a leading cause of cancer death. This study aimed to investigate the key role of miR-21-3p in CRC by inhibiting its expression using transfection with miR-21-3p inhibitors into human CRC HCT116 cells. Results showed that the expression of miR-21-3p was higher than other CRC cells used in the study including Lovo, HT29, Colo320 and SW480 cells, inhibition of which suppressed the proliferation and induced cell cycle arrest in HCT116 cells. Besides, transfection with miR-21-3p inhibitors also attenuated cell migration and invasion, and induced apoptosis as well. Moreover, luciferase assay confirmed RBPMS as a direct target of miR-21-3p in HCT116 cells. Further, miR-21-3p inhibitors increased the nuclear accumulation of Smad4 and reduced phosphorylation of ERK. Interestingly, we found that silence of RBPMS using RNA interference (siRNA) not only elevated the cell viability but also increased the phosphorylation of ERK and reversed the nuclear accumulation of Smad4 induced by miR-21-3p inhibitors in HCT116 cells. Data suggest that inhibition of miR-21-3p suppresses cell proliferation, invasion as well as migration and induces apoptosis by directly targeting RBPMS through Smad4/ERK signalling pathway in HCT116 cells. Our study demonstrates miR-21-3p as a potent target for suppressing tumour progression of CRC which may have implications in CRC therapy in the future.

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Targeting miR-21-3p inhibits proliferation and invasion of ovarian cancer cells

Cited by 93 publications

References 35 publications

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Inhibition of microRNA‐21‐3p suppresses proliferation as well as invasion and induces apoptosis by targeting RNA‐binding protein with multiple splicing through Smad4/extra cellular signal‐regulated protein kinase signalling pathway in human colorectal cancer HCT116 cells

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