LINC00511 promotes gastric cancer cell growth by acting as a ceRNA

Sun, Chao; Wang, Hongyi; Han, Xiaoqing; Liu, Yongning; Wang, Mengchun; Zhang, Hongxia; Gu, You-Feng; Leng, Xiaogang

doi:10.4251/wjgo.v12.i4.394

Cited by 31 publications

(23 citation statements)

References 28 publications

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“…Long non-coding RNAs (LncRNAs) are participated in modulating the tumorigenesis and progression of many human cancers, [6][7][8] including EC. [9][10][11] For instance, overexpression of LINC-ROR is reported to promote the growth of EC.…”

Section: Introductionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Gao¹,

Yu²,

Zhang³

et al. 2020

OTT

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Endometrial cancer (EC) is an aggressive tumor in females and the development of EC is considered to regulate by some long non-coding RNAs (lncRNAs). Therefore, this study aimed to investigate the regulatory mechanism of lncRNA LINC01106 on EC. Methods: The expression of lncRNA LINC01106, miR-449a and MET in EC tissues and cells was detected by qRT-PCR. Through MTT, wound healing and transwell invasion assays, the proliferation, migration and invasion of EC cells were detected, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibiting effect of LINC01106 knockdown on EC in vivo. The interactions between miR-449a and LINC01106/ MET were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein level of MET. Results: LncRNA LINC01106 expression was highly up-regulated in EC tissues and cells. The proliferation, migration and invasion of EC cells in vitro were inhibited by the transfection of sh-LINC01106. The growth of tumor xenograft was suppressed by injection of sh-LINC01106. MiR-449a was a target of LINC01106and was negatively modulated by LINC01106. MiR-449a overexpression suppressed the proliferation, migration and invasion of EC cells. In addition, MET was identified as a target gene of miR-449a. Both the high expression of miR-449a and low expression of MET reversed the inhibiting effects of LINC01106 knockdown on Ishikawa cells. Conclusion: Silencing of LINC01106 inhibits the occurrence and development of EC via regulating the miR-449a/MET axis. This study provides a possible therapeutic strategy for EC.

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Section: Introductionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Gao¹,

Yu²,

Zhang³

et al. 2020

OTT

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“…The -untreated BGC-823 cells were set up as the blank group. BGC-823 were respectively transfected with si-NC, si-circ_0000654, oe-circ_0000654, oe-NC, NC-mimic, miR-149-5p-mimic, si-circ_0000654 + NC-inhibitor, and si-circ_0000654 + miR-149-5p-inhibitor using Lipofectamine 2000 (Invitrogen) [ 19 ]. The plasmids or oligonucleotides were synthesized by GenePharma (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

“…Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and U6 were used for internal control. Gene levels were analyzed through 2 −ΔΔCt method [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

Circular RNA 0000654 facilitates the growth of gastric cancer cells through absorbing microRNA-149-5p to up-regulate inhibin-beta A

Liu

Dai

2022

Bioengineered

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Circular (circ) RNAs are differentially expressed in gastric cancer (GC) and participate in the biological growth of tumor cells. Given that, investigations were performed to unravel the function of circ_0000654 in GC. GC tissue and normal tissue specimens were obtained, in which circ_0000654, microRNA (miR)-149-5p, and inhibin-beta A (INHBA) levels were examined. GC cell line (BGC-823) was transfected to alter circ_0000654 and miR-149-5p expression, thereby observing cell malignancy. Stably-transfected BGC-823 cells were injected into nude mice to observe tumor growth in vivo . The interaction circ_0000654, miR-149-5p, and INHBA was validated. circ_0000654 and INHBA were up-regulated but miR-149-5p was down-regulated in GC. circ_0000654 absorbed miR-149-5p to target INHBA. Silencing circ_0000654inhibited the progress of GC cell biology. Oppositely, restoring circ_0000654 enhanced the growth of GC cells. Inhibiting miR-149-5p rescued down-regulated circ_0000654-induced anti-tumor effect on GC. circ_0000654 silence or miR-149-5p overexpression limited the growth of GC tumors in vivo . Obviously, circ_0000654 facilitates the growth of GC cells through absorbing miR-149-5p to up-regulate INHBA.

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“…In recent years, accumulating studies find that long non-coding RNAs (lncRNAs) are aberrantly expressed in diverse tumors, which is involved in tumorigenesis and disease development [6,7]. For instance, lncRNA TPTEP1, SPRY4-IT1 and ZEB2-AS1 are reported to be aberrantly expressed in NSCLC and modulate biological processes such as proliferation and metastasis of cancer cells [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MCM3AP antisense RNA 1 promotes non-small cell lung cancer progression through targeting microRNA-195-5p

Shen

Tao

et al. 2021

Bioengineered

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Lung cancer (LC) ranks first among all causes of cancer-related death, with non-small cell lung cancer (NSCLC) taking up 85% of lung cancer cases. Although lncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) has been reported to be an oncogenic factor in NSCLC, its detailed mechanism in NSCLC is unknown. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine MCM3AP-AS1, microRNA (miR)-195-5p and E2F transcription factor 3 (E2F3) mRNA expressions in NSCLC tissues and cells. Western blot was utilized to determine the expression levels of E2F3, BCL2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), E-cadherin and N-cadherin. CCK-8 and Transwell assays were conducted to examine cell proliferation, migration and invasion, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation experiments were used to determine the regulatory relationships between MCM3AP-AS1 and miR-195-5p, and miR-195-5p and E2F3. We demonstrated that MCM3AP-AS1 was overexpressed in NSCLC tissues and cells, and MCM3AP-AS1 overexpression accelerated the proliferation, migration and invasion of NSCLC cells. In addition, MCM3AP-AS1 overexpression markedly up-modulated Bcl-2 expression and repressed Bax expression; MCM3AP-AS1 overexpression also significantly upregulated N-cadherin expression and suppressed E-cadherin expression in NSCLC cells. What is more, in NSCLC cells, miR-195-5p was a target of MCM3AP-AS1, and the latter worked as a molecular sponge for miR-195-5p to regulate E2F3 expression. Collectively, MCM3AP-AS1, serving as a competitive endogenous RNA (ceRNA) to regulate miR-195-5p/E2F3 axis, promotes NSCLC progression, which is a promising therapeutic target for NSCLC.

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LINC00511 promotes gastric cancer cell growth by acting as a ceRNA

Cited by 31 publications

References 28 publications

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Circular RNA 0000654 facilitates the growth of gastric cancer cells through absorbing microRNA-149-5p to up-regulate inhibin-beta A

Long non-coding RNA MCM3AP antisense RNA 1 promotes non-small cell lung cancer progression through targeting microRNA-195-5p

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