MicroRNA‐492 overexpression involves in cell proliferation, migration, and radiotherapy response of cervical squamous cell carcinomas

Liu, Mei; An, Jusheng; Huang, Manni; Wang, Liming; Tu, Binbin; Song, Yan; Ma, Kai; Wang, Yu; Wang, Shuren; Zhu, Hongxia; Xu, Nuo; Wu, Lingying

doi:10.1002/mc.22717

Cited by 28 publications

(30 citation statements)

References 35 publications

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“…miR-492 is aberrantly expressed in several types of human cancer. For example, miR-492 is downregulated in cervical cancer tissue specimens and cell lines (20). miR-492 downregulation is significantly correlated with the pelvic lymph node metastasis of patients with cervical cancer (20).…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Sun

Zhang

2018

Mol Med Report

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Numerous studies have demonstrated that microRNAs (miRNAs) are upregulated or downregulated in retinoblastoma (RB), and that this phenomenon is associated with the modulation of various malignant behaviours during RB occurrence and development. Therefore, the mechanisms that associate deregulated miRNAs with RB initiation and progression must be understood to identify effective therapeutic techniques for patients with RB. In the present study, miR-492 expression was upregulated in RB tissues and cell lines. The effects of miR-492 inhibition on the proliferation and invasion of RB cells were examined using Cell Counting kit-8 and invasion assays. The results revealed that miR-492 downregulation significantly decreased the proliferation and invasion of RB cells. Bioinformatics analysis predicted that large tumour-suppressor kinase 2 (LATS2) was a putative target of miR-492. Luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction and western blot analysis demonstrated that LATS2 was a direct target gene of miR-492 in RB cells. In addition, LATS2 expression was downregulated in RB tissues, and its downregulation was inversely correlated with miR-492 level. Furthermore, LATS2-knockdown abrogated the effects of miR-492 downregulation in RB cells. In conclusion, miR-492 inhibition may impede the malignant behaviour of RB by directly targeting LATS2. Therefore, targeting this miRNA may be an effective therapeutic method for treating patients with RB.

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Section: Discussionmentioning

confidence: 99%

“…Therefore, miRNAs may serve as potential diagnostic biomarkers and therapeutic targets for patients with RB. miR-492 is reportedly downregulated in cervical cancer (20), osteosarcoma (21) and clear cell renal cell carcinoma (22). By contrast, miR-492 is upregulated in hepatoblastoma, hepatic cancer (23) and breast cancer (24).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Sun

Zhang

2018

Mol Med Report

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“…Thus, it is clear that MMP develops a pleiotropic effect on tumor installation by remodeling ECM and activating signaling molecules, impacting cell adhesion and metastatic phenotype ( Figure 5). [78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93] Studies suggested that MMPs are involved in initial step of ECM degradation during metastatic process. 5,22,40,72…”

Section: Mmps Timps Referencesmentioning

confidence: 99%

“…Xiao, et al 93 (2015) Figure 5-Summary of the miRNAs effect over MMPs in some diseases [78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93] Updating the role of matrix metalloproteinases in mineralized tissue and related diseases J Appl Oral Sci. 2019;27:e20180596 9/14 also important in genes encoding MMPs and they lead to changes in MMP expression patterns in cancer.…”

Section: Colorectal Cancermentioning

confidence: 99%

Updating the role of matrix metalloproteinases in mineralized tissue and related diseases

et al. 2019

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Updating the role of matrix metalloproteinases in mineralized tissue and related diseases Bone development and healing processes involve a complex cascade of biological events requiring well-orchestrated synergism with bone cells, growth factors, and other trophic signaling molecules and cellular structures. Beyond health processes, MMPs play several key roles in the installation of heart and blood vessel related diseases and cancer, ranging from accelerating metastatic cells to ectopic vascular mineralization by smooth muscle cells in complementary manner. The tissue inhibitors of MMPs (TIMPs) have an important role in controlling proteolysis. Paired with the post-transcriptional efficiency of specific miRNAs, they modulate MMP performance. If druggable, these molecules are suggested to be a platform for development of "smart" medications and further clinical trials. Thus, considering the pleiotropic effect of MMPs on mammals, the purpose of this review is to update the role of those multifaceted proteases in mineralized tissues in health, such as bone, and pathophysiological disorders, such as ectopic vascular calcification and cancer. Bone is a specialized, vascular, and dynamic connective tissue in constant remodeling to maintain physiological ion homeostasis, give support and protection for soft tissue, and be a reservoir of ions important to vertebrates. 1-3 Mechanistically, bone remodeling requires a coordinate and dynamic relationship between deposition/degradation of extracellular matrix (ECM), through growth factors and other signaling molecules, which results in ECM remodeling-an important prerequisite for cell adhesion, migration, proliferation, differentiation. 4 It is well known that osteoclasts resorb the mineralized matrix and further promote the remodeling of the organic fraction of the bone, while, conversely, osteoblasts are responsible for bone formation by depositing specialized ECM components prior to mineralizing it properly 2 . The balance between those specialized cells is crucial for maintaining appropriate bone mass, and the lack of this synchronism contributes to the occurrence of bone diseases, such as osteoporosis and Paget's. To date, ultimate bone cellular differentiation is known to depend on wellorchestrated communication between formation and resorption events. 2,5-7 More specifically, during bone repair after trauma, bone healing depends on interactions between specific signaling inflammatory cytokines and non-resident and eventual cells (such as polymorphonuclear leukocytes and monocyte-macrophage lineage), 8 requiring ECM remodeling by specific matrix metalloproteinases (MMPs). Generally, MMPs are an important family of zinc-dependent endopeptidases and are the major class of enzymes responsible for the degradation or resorption of all ECM components (Figure 1). 9-15 MMP targets include other proteases, protease inhibitors, blood coagulation factors, chemotactic molecules, latent growth factors, binding protein growth factor, cell surface receptors, and cell adhesion molecule...

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“…The previous studies has reported that miR-492 was involved in the development of some cancers, such as cervical squamous cell carcinomas [21], hepatoblastoma [22] and colon cancer cells [23]. We chose different types of cancer cell lines to detect the expression of miR-492.…”

Section: Mir-492 Promoted the Cell Proliferation Of Endometrial Cancementioning

confidence: 99%

Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

Chang

Hao

Jia

et al. 2020

Preprint

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Background: Endometrial cancer is the prevalent invasive gynecological cancer in the world. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Metapristone is a hormone related drug and widely used in endometrial cancer clinical therapeutics. However, the deep regulatory mechanism of metapristone is not clear. In this research, we aimed to figure out the specific molecular mechanism during the treatment of endometrial cancer with metapristone.Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. Moreover, the mice tumor model was used to confirm the function of metapristone and the regulating process by miR-492/Klf5/Nrf1 axis in vivo. The protein expression was measured by western blot. Cell proliferation and apoptosis was monitored using the MTT assay, cell colony formation assay and EdU assay.Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

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MicroRNA‐492 overexpression involves in cell proliferation, migration, and radiotherapy response of cervical squamous cell carcinomas

Cited by 28 publications

References 35 publications

Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Updating the role of matrix metalloproteinases in mineralized tissue and related diseases

Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

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