&lt;p&gt;Effect of miR-515-5p on Proliferation and Drug Sensitivity of Retinoblastoma Cells&lt;/p&gt;

Yuan, Xiang Wen; Yan, Ting; Tong, Huilin

doi:10.2147/cmar.s271165

Cited by 20 publications

(11 citation statements)

References 45 publications

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“…And overexpression of miR‐515‐5p inhibited the proliferation, invasion, and metastasis of liver cancer cells by regulating the IL‐6/JAK/STAT3 signaling pathway (Ni et al, 2020). However, Yuan indicated that miR‐515‐5p overexpression could inhibit the proliferation and drug resistance of retinoblastoma cells by targeted downregulation of Notch1 expression (Yuan et al, 2020). Moreover, miR‐515‐3p had low expression in esophageal squamous cell carcinoma tissues and even lower expression in tumor tissues of metastatic patients.…”

Section: Discussionmentioning

confidence: 99%

Targeting of MAD2L1 by miR‐515‐5p involves the regulation of cell cycle arrest and apoptosis of colorectal cancer cells

Ding

Chen

et al. 2022

Cell Biology International

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Although many previous studies have found that the mitotic arrest deficient 2-like 1 (MAD2L1) protein contributes to the proliferation of colorectal cancer (CRC) cells, but the upstream mechanism of MAD2L1 is still largely elusive. This study aimed to explore the microRNAs (miRNAs) upstream of MAD2L1 to improve our understanding of the mechanism of the MAD2L1 gene in CRC. The upstream target miRNAs (miR-515-5p) of MAD2L1 were predicted by the online databases miRWalk, miRDIP, and TargetScan. Quantitative real-time PCR (qRT-PCR) was used to detect the expression level of miR-515-5p in human CRC tissues. The targeting relationship between miR-515-5p and MAD2L1 was tested by dual luciferase reporter gene assays. The effects of miR-515-5p on the biological behaviors of CRC cells by regulating MAD2L1 expression were verified by qRT-PCR, western blot, Cell Counting Kit-8, and flow cytometry. The results showed that miR-515-5p was a highly reliable upstream miRNA of the MAD2L1 gene. As an upstream target miRNA of MAD2L1, miR-515-5p was lowly expression in CRC tissues. The overexpression of miR-515-5p could inhibit the proliferation of CRC cells and induce cell cycle arrest at the G1 phase leading to cell apoptosis. However, MAD2L1 gene overexpression could reverse the effects of miR-515-5p overexpression on the biological behaviors of CRC cells above. This study illustrated that miR-515-5p can inhibit proliferation and induce G1 phase arrest leading to apoptosis in CRC cells. The mechanism underlying this phenomenon may be related to the negative targeted regulation of MAD2L1.

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Section: Discussionmentioning

confidence: 99%

Targeting of MAD2L1 by miR‐515‐5p involves the regulation of cell cycle arrest and apoptosis of colorectal cancer cells

Ding

Chen

et al. 2022

Cell Biology International

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“…Relative to circKIF4A, miR-515-5p expressions were markedly decreased in OS, further verifying the combination of the two. miR-515-5p inhibits various cancer processes, for instance, it acts as a prostate cancer inhibitor by targeting TRIP13 [25], suppresses HCC migration as well as invasion via the IL6/JAK/STAT3 pathway [26], inhibits breast cancer cell proliferation, migration as well as invasion via the hsa_circ_0008039/miR-515-5p/CBX4 axis [27]. The functions of miR-515-5p in OS is basically the same as the above researches.…”

Section: Discussionmentioning

confidence: 89%

CircKIF4A Enhances Osteosarcoma Proliferation And Metastasis By Sponging MiR-515-5p And Upregulating SLC7A11

Feng

Wang

et al. 2021

Preprint

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Background Circular RNAs (circRNAs) are forms of non-coding RNAs that have crucial roles in regulation of various biological processes of several malignant tumors. circKIF4A is closely associated with malignant progression of a variety of cancers. However, the molecular mechanisms as well as roles of circKIF4A in osteosarcoma (OS) have not yet been clearly elucidated. Methods We evaluated the expression of circKIF4A in OS. Colony-formation, cell counting kit-8 (CCK-8), transwell and mice metastasis model assays were done to explore the roles of circKIF4A in vitro and in vivo. TargetScan database, double luciferase, quantitative reverse transcription polymerase chain reaction analysis (RT-qPCR), and RNA immunoprecipitation (RIP) were done to investigate the associated molecular mechanisms. Results In both OS cells and tissues, circKIF4A (hsa_circ_0007255) was found to be upregulated. In vitro and in vivo, circKIF4A knockdown markedly suppressed OS proliferation as well as metastasis. circKIF4A enhanced OS growth as well as metastasis by sponging miR-515-5p and by upregulating SLC7A11. Conclusions We identified the biological significance of the circKIF4A-miR-515-5p-SLC7A11 axis in OS cell proliferation and metastasis, which is important in OS monitoring and treatment. More studies on circKIF4A will inform on the diagnostic markers for early OS screening.

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“…HOTAIR propels carcinogenesis and shows an association with tumor initiation and progression, drug resistance, and poor survival rates of patients [ 28 ]. In previous studies concerning RB, most researchers have selected ARPE-19 cells as the control group [ 29 – 31 ]. The results of our study found no significant difference in HOTAIR expression between the two normal retinal cell lines ARPE-19 and RPE-1, and thus ARPE-19 cells could be utilized as the ideal control in our experiments.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR facilitates proliferation and represses apoptosis of retinoblastoma cells through the miR-20b-5p/RRM2/PI3K/AKT axis

Zhang

2022

Orphanet J Rare Dis

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Purpose Retinoblastoma (RB) represents an adolescent eye malignancy. Long non-coding RNA (LncRNA) HOTAIR shows aberrant expression in many malignancies. This research investigated the mechanism of HOTAIR in RB. Methods Normal retinal cell lines (ARPE-19 and RPE-1) and RB cell lines (ORB50, Y79, HXO-RB44, and WERI-RB) were selected for detection of HOTAIR expression by qRT-PCR. sh-HOTAIR was delivered into Y79 and HXO-RB44 cells. Cell-cycle distribution, proliferation, and apoptosis were detected by CCK-8 assay and flow cytometry. Binding relationships among HOTAIR, miR-20b-5p, and RRM2 were confirmed using dual-luciferase assay. Roles of miR-20b-5p and RRM2 in RB cell-cycle distribution, proliferation, and apoptosis were ascertained by functional rescue experiments. Murine model of xenograft tumor was established, followed by detection of tumor growth and counting of Ki67-positive cells. Expressions of proliferation- and apoptosis-associated proteins and PI3K/AKT pathway-related proteins were determined by Western blot. Results HOTAIR was elevated in RB cells relative to that in normal retinal cells and showed relatively high expression in Y79 and HXO-RB44 cells. sh-HOTAIR induced RB cell-cycle arrest, restrained proliferation, and strengthened apoptosis. HOTAIR functioned as the ceRNA of miR-20b-5p and targeted RRM2. RB cells had poorly-expressed miR-20b-5p and highly-expressed RRM2. miR-20b-5p downregulation or RRM2 overexpression facilitated RB cell-cycle and proliferation, suppressed apoptosis, and reversed the protective effect of sh-HOTAIR on RB. sh-HOTAIR reduced tumor growth and Ki67-positive cells in vivo and inactivated PI3K/AKT pathway. Conclusion LncRNA HOTAIR upregulated RRM2 by competitively binding to miR-20b-5p and activated PI3K/AKT pathway, thereby facilitating proliferation and repressing apoptosis of RB cells.

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<p>Effect of miR-515-5p on Proliferation and Drug Sensitivity of Retinoblastoma Cells</p>

Cited by 20 publications

References 45 publications

Targeting of MAD2L1 by miR‐515‐5p involves the regulation of cell cycle arrest and apoptosis of colorectal cancer cells

Targeting of MAD2L1 by miR‐515‐5p involves the regulation of cell cycle arrest and apoptosis of colorectal cancer cells

CircKIF4A Enhances Osteosarcoma Proliferation And Metastasis By Sponging MiR-515-5p And Upregulating SLC7A11

LncRNA HOTAIR facilitates proliferation and represses apoptosis of retinoblastoma cells through the miR-20b-5p/RRM2/PI3K/AKT axis

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