Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Yan, Guigang; Su, Yi; Ma, Zhao; Yu, Lianzhi; Chen, Ning

doi:10.1247/csf.18033

Cited by 30 publications

(19 citation statements)

References 28 publications

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“…For instance, the low expression of miR-125a-5p in RB promoted cell growth [14]. The similar results about miR-3619-5p [6], miR-492 [15], and miR-758 [16] were also found in RB. MiR-655-3p has been reported to impact cell behaviors of tumor progression in ovarian cancer [17], non-small cell lung cancer [18].…”

supporting

confidence: 56%

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Long non-coding RNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression by sponging miR-655-3p

Zhao¹,

Wang²,

Gao³

et al. 2020

Preprint

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Background: Long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB.Methods: The levels of MALAT1, microRNA-655-3p (miR-655-3p), and ATPase family AAA domain containing 2 (ATAD2) in RB tissues and cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and apoptotic rate were monitored via cell counting kit 8 (CCK8) assay and flow cytometry, respectively. The protein levels of p21, CyclinD1, B-cell lymphoma-2 (Bcl-2), cleaved-casp-3, E-cadherin, Ncadherin, Vimentin, and ATAD2 were detected by Western blot assay. Transwell assay was performed to estimate the abilities of migration and invasion. The interactions between miR-655-3p and MALAT1 or ATAD2 were predicted by starBase. Dual-luciferase reporter assay was constructed to verify these interactions. The mice model experiments were established to validate the effects of MALAT1 in vivo.Results: MALAT1and ATAD2 were significantly increased while the level of miR-655-3p was remarkably decreased in RB tissues and cells. MALAT1 knockdown inhibited cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT) but promoted apoptosis via miR-655-3p in vitro, and blocked xenograft tumor growth in vivo. MALAT1 was validated to sponge miR-655-3p and ATAD2 was verified as a candidate of miR-655-3p. MiR-655-3p overexpression inhibited cell proliferation but promoted apoptosis by targeting ATAD2. MALAT1 silencing affected cell behaviors by regulating ATAD2. MALAT1 depletion down-regulated ATAD2 expression via miR-655-3p in RB cells.Conclusion: MALAT1 positively regulated ATAD2 to accelerate cell proliferation but retard apoptosis by sponging miR-655-3p in RB cells.

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supporting

confidence: 56%

“…Many lncRNAs were reported to be dysregulated in RB and regulate biological processes in the tumor. For example, LINC00202 was highly expressed in RB, and its silencing retarded cell growth, metastasis in vitro [6]. THOR was up-regulated in RB, the depletion of THOR resulted in the decrease of cell growth, metastasis, and the increase of apoptosis [7].…”

mentioning

confidence: 99%

Long non-coding RNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression by sponging miR-655-3p

Zhao¹,

Wang²,

Gao³

et al. 2020

Preprint

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“…Compelling evidence indicates that miR-3619-5p could suppress β-catenin-mediated cancer growth and invasion in non-small cell lung cancer cells (34). In support of these findings, decreased miR-3619-5p expression has been detected in retinoblastoma cells, and transfection with miR-3619-5p mimic can improve the progression of retinoblastoma (35). In the present study, miR-3619-5p inhibitor reversed the effects of LINC00958 silencing on proliferation, invasion, migration and apoptosis of CRC cells.…”

Section: Discussionmentioning

confidence: 65%

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

et al. 2020

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The aberrant expression of long non-coding RNAs (lncRNAs), including LINC00958, has been demonstrated in several types cancers. The present study aimed to investigate the role of LINC00958 in colorectal cancer (CRC) and identify the possible underlying mechanisms. The expression of LINC00958 and microRNA (miR)-3619-5p was detected in several human CRC cell lines using reverse transcription-quantitative PCR. Then, short hairpin RNA (shRNA)-LINC00958 was transfected into the cells. The results revealed that the expression of LINC00958 was notably upregulated, whereas miR-3619-5p was downregulated in CRC cells. Transfection with shRNA-LINC00958 inhibited the proliferation, invasion and migration of CRC cells. Moreover, the rate of apoptosis was enhanced, accompanied by a decrease in the expression of Bcl-2 and an increase in the expression of Bax and caspase-3. A luciferase reporter assay was conducted to verify the target binding site between LINC00958 and miR-3619-5p. The luciferase reporter assay confirmed that miR-3619-5p could be directly targeted by LINC00958. Furthermore, the miR-3619-5p inhibitor reversed the effects of LINC00958 silencing on proliferation, invasion, migration and apoptosis. Taken together, the findings suggest that the downregulation of LINC00958 suppresses the proliferation, invasion and migration, and promotes the apoptosis of CRC cells by targeting miR-3619-5p in vitro, which provides a theoretical basis and therapeutic strategy for the treatment of CRC.

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“…Previous studies indicated that miR-3619-5p inhibits cell proliferation and migration in HCC [34]. miR-3619-5p is involved in LINC00202-mediated retinoblastoma progression through targeting the expression of an oncogene RIN1 [35]. miR-3619-5p has also been demonstrated to exert a tumor-suppressive role in several types of malignancies, including bladder cancer [36], lung cancer [37], prostate cancer [38], and cutaneous squamous cell carcinoma [39].…”

Section: Discussionmentioning

confidence: 99%

M6A-mediated upregulation of LINC00958 increases lipogenesis and acts as a nanotherapeutic target in hepatocellular carcinoma

et al. 2020

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Background: Long non-coding RNAs (lncRNAs) possess significant regulatory functions in multiple biological and pathological processes, especially in cancer. Dysregulated lncRNAs in hepatocellular carcinoma (HCC) and their therapeutic applications remain unclear.Methods: Differentially expressed lncRNA profile in HCC was constructed using TCGA data. LINC00958 expression level was examined in HCC cell lines and tissues. Univariate and multivariate analyses were performed to demonstrate the prognostic value of LINC00958. Loss-of-function and gain-of-function experiments were used to assess the effects of LINC00958 on cell proliferation, motility, and lipogenesis. Patient-derived xenograft model was established for in vivo experiments. RNA immunoprecipitation, dual luciferase reporter, biotin-labeled miRNA pulldown, fluorescence in situ hybridization, and RNA sequencing assays were performed to elucidate the underlying molecular mechanisms. We developed a PLGA-based nanoplatform encapsulating LINC00958 siRNA and evaluated its superiority for systemic administration. Results:We identified a lipogenesis-related lncRNA, LINC00958, whose expression was upregulated in HCC cell lines and tissues. High LINC00958 level independently predicted poor overall survival. Functional assays showed that LINC00958 aggravated HCC malignant phenotypes in vitro and in vivo. Mechanistically, LINC00958 sponged miR-3619-5p to upregulate hepatoma-derived growth factor (HDGF) expression, thereby facilitating HCC lipogenesis and progression. METTL3-mediated N 6 -methyladenosine modification led to LINC00958 upregulation through stabilizing its RNA transcript. A PLGA-based nanoplatform loaded with si-LINC00958 was developed for HCC systemic administration. This novel drug delivery system was controlled release, tumor targeting, safe, and presented satisfactory antitumor efficacy.

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Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Cited by 30 publications

References 28 publications

Long non-coding RNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression by sponging miR-655-3p

Long non-coding RNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression by sponging miR-655-3p

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

M6A-mediated upregulation of LINC00958 increases lipogenesis and acts as a nanotherapeutic target in hepatocellular carcinoma

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