lncRNA PCAT18 inhibits proliferation, migration and invasion of gastric cancer cells through miR-135b suppression to promote CLDN11 expression

Zhang, Xiaozhan; Mao, Hongli; Zhang, Shijie; Sun, Li; Zhang, Wenjing; Chen, Qingzhou; Wang, Lei; Liu, Hongchun

doi:10.1016/j.lfs.2020.117478

Cited by 28 publications

(13 citation statements)

References 28 publications

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“…21 PCAT18 has been found to sponge miR-107 and miR-135b in gastric cancer. 11,12 We also found that PCAT18 was expressed in the cytoplasm of CRC cells, suggesting it may be also a miRNA sponge. Through bioinformatics prediction, we identified miR-759 as the target.…”

Section: Discussionmentioning

confidence: 58%

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<p>Long Noncoding RNA PCAT18 Upregulates SPRR3 to Promote Colorectal Cancer Progression by Binding to miR-759</p>

Yang

Xia

et al. 2020

CMAR

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Background: Long noncoding RNAs (lncRNAs) play essential functions in the development of several cancers, including colorectal cancer (CRC). Nevertheless, how PCAT18 regulates CRC tumorigenesis remains unclear. In this research, we aimed to investigate the roles of PCAT18 in CRC. Materials and Methods: qRT-PCR and Western blot were used to analyze RNA and protein levels. CCK8, colony formation, transwell and wound healing assays were utilized to analyze proliferation, migration and invasion. Luciferase reporter assay was used to analyze RNA interactions. Results: PCAT18 was found to be highly expressed in CRC tissues and cells. PCAT18 level was positively correlated with lymph node metastasis and TNM stage. Functionally, PCAT18 silencing induced impairment of CRC proliferation, migration and invasion. Besides, PCAT18 was identified to inhibit miR-759. PCAT18 promotes SPRR3 expression through binding to miR-759. Furthermore, miR-759 inhibitors or SPRR3 ectopic expression partially rescued the abilities of proliferation, migration and invasion in CRC cells transfected with sh-PCAT18. Conclusion: Therefore, our study demonstrated that PCAT18 contributes to CRC progression through regulating miR-759/SPRR3 axis, which provides a new theoretical basis of explaining CRC tumorigenesis.

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Section: Discussionmentioning

confidence: 58%

“…LncRNA PCAT18 has been shown to inhibit gastric cancer progression. 11 Another study also confirms the inhibitory role of PCAT18 in gastric cancer. 12 Nevertheless, the role of PCAT18 in CRC remains unclear.…”

Section: Introductionmentioning

confidence: 70%

<p>Long Noncoding RNA PCAT18 Upregulates SPRR3 to Promote Colorectal Cancer Progression by Binding to miR-759</p>

Yang

Xia

et al. 2020

CMAR

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“…Xiao et al 37 showed that TRPM2-AS enhanced gastric tumor radioresistance and progression via sponging miR-612. Zhang et al 38…”

Section: Discussionmentioning

confidence: 99%

“…showed that TRPM2‐AS enhanced gastric tumor radioresistance and progression via sponging miR‐612. Zhang et al 38 . indicated that PCAT18 suppressed invasion, growth and migration by modulating CLDN11/miR‐135b in gastric tumor.…”

Section: Discussionmentioning

confidence: 99%

LINC00689 induces gastric cancer progression via modulating the miR‐338‐3p/HOXA3 axis

Zhang

Sun

et al. 2020

The Journal of Gene Medicine

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Background: LINC00689 acts one critical regulatory role in several tumors. However, the functional, regulatory mechanism and expression of LINC00689 remains unknown in gastric cancer. Methods: LINC00689 and miR-338-3p levels were determined using a quantitative reverse transcriptase-polymerase chain reaction analysis and an enzyme-linked immunoassay and a cell-counting kit-8 assay were utilized to detect interleukin (IL)-8, IL-6 and IL-1β expression and cell proliferation, respectively. Results: We found that LINC00689 and HOXA3 are overexpressed and miR-338-3p is decreased in gastric cancer cells. Compared to control specimens, LINC00689 is overexpressed in gastric cancer specimens and the level of LINC00689 was up-regulated in 32 cases (32/40; 80.0%) compared to control samples. LINC00689 increased cell growth, epithelial-mesenchymal transition (EMT) development and secretion of inflammatory factors in gastric cancer. Compared to control specimens, miR-338-3p expression was decreased in gastric cancer specimens and a Pearson's correlation assay revealed that miR-338-3p was negatively correlated with LINC00689 expression in gastric cancer specimens. HOXA3 was identified as one target gene of miR-338-3p and Ectopic expression of LINC00689 suppressed miR-338-3p and enhanced HOXA3 expression in HGC-27 cells. LINC00689 enhanced cell growth, EMT development and secretion of inflammatory factors by promoting HOXA3. Conclusions: LINC00689 may present a potential future target for gastric cancer treatment.

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“…It was reported that PCAT18 inhibited gastric cancer progression. 11 , 12 Nevertheless, Yang et al reported the oncogenic role of PCAT18 in colorectal cancer. 13 Obviously, the biological effects and underlying mechanism of PCAT18 in the development of main human cancers, including NSCLC, remain elusive.…”

Section: Introductionmentioning

confidence: 99%

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

Wang²,

Zhou

et al. 2021

CMAR

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Introduction NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development. Methods The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319. Results PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo. Conclusion In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.

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lncRNA PCAT18 inhibits proliferation, migration and invasion of gastric cancer cells through miR-135b suppression to promote CLDN11 expression

Cited by 28 publications

References 28 publications

<p>Long Noncoding RNA PCAT18 Upregulates SPRR3 to Promote Colorectal Cancer Progression by Binding to miR-759</p>

<p>Long Noncoding RNA PCAT18 Upregulates SPRR3 to Promote Colorectal Cancer Progression by Binding to miR-759</p>

LINC00689 induces gastric cancer progression via modulating the miR‐338‐3p/HOXA3 axis

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

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