LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

Luan, Xiaotian; Wang, Yankui

doi:10.3802/jgo.2018.29.e95

Cited by 166 publications

(145 citation statements)

References 46 publications

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“…Generally, miRNAs exert their functions by direct cleavage and/or translational inhibition of target mRNAs. Recently, it has been reported that miR‐331‐3p has several targets in different cancers, such as PHLPP in hepatocellular cancer, ST7L in pancreatic cancer and NRP2 in cervical cancer . ErbB2 was also reported to be a target of miR‐331‐3p, but the signaling pathway that was regulated by miR‐331‐3p that targeted ErbB2 was unknown.…”

Section: Discussionmentioning

confidence: 99%

“…14 However, other researchers discovered antitumor functions of miR-331-3p in urothelial cancer, 29 gastric cancer, 16 and cervical cancer. 17 The functions of miR-331-3p in NSCLC were also ambiguous, 30 14 and NRP2 in cervical cancer. 17 ErbB2 was also reported to be a target of miR-331-3p, 16 but the signaling pathway that was regulated by miR-331-3p that targeted ErbB2 was unknown.…”

Section: Discussionmentioning

confidence: 99%

“…17 The functions of miR-331-3p in NSCLC were also ambiguous, 30 14 and NRP2 in cervical cancer. 17 ErbB2 was also reported to be a target of miR-331-3p, 16 but the signaling pathway that was regulated by miR-331-3p that targeted ErbB2 was unknown. Our results confirmed the regulation of miR-331-3p on ErbB2 and discovered that VAV2 was a novel direct target of miR-331-3p.…”

Section: Discussionmentioning

confidence: 99%

“…However, the effect of miR‐331‐3p in different cancer types completely varies. MiR‐331‐3p functions as an oncogene in pancreatic cancer and hepatocellular cancer, but as a tumor suppressor gene in gastric cancer and cervical cancer . Although these studies described the effects of miR‐331‐3p in different types of cancer, the biological functions of miR‐331‐3p in NSCLC are still unknown.…”

Section: Introductionmentioning

confidence: 99%

“…MiR-331-3p functions as an oncogene in pancreatic cancer 14 and hepatocellular cancer, 15 but as a tumor suppressor gene in gastric cancer 16 and cervical cancer. 17 Although these studies described the effects of miR-331-3p in different types of cancer, the biological functions of miR-331-3p in NSCLC are still unknown. Herein, we found that the expression level of miR-331-3p was significantly lower in NSCLC tumor tissues than in adjacent normal tissues and negatively correlated with advanced stage and lymph node metastasis of NSCLC.…”

mentioning

confidence: 99%

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MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Zhu

Liu

et al. 2019

Cancer Science

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MicroRNAs have been reported to play critical roles in the regulation of non‐small‐cell cancer (NSCLC) development, but the role of microRNA (miR)‐331‐3p in NSCLC is still unclear. In this study, the expression levels of miR‐331‐3p in NSCLC tumor tissues and adjacent normal tissues were examined by quantitative RT‐PCR, and the relationship between miR‐331‐3p expression and patient clinicopathological characteristics was analyzed. The effects of miR‐331‐3p on epithelial‐mesenchymal transition (EMT), migration, and metastasis of NSCLC cells were determined in vitro and vivo. Direct functional targets of miR‐331‐3p were identified by luciferase reporter assay, western blot assay, immunohistochemical staining, and rescue assay. The downstream pathway regulated by miR‐331‐3p was identified by immunofluorescence, immunoprecipitation, and Rac1 activity examination. Our results showed that miR‐331‐3p was significantly downregulated in NSCLC tumor tissues and was correlated with clinicopathological characteristics, and miR‐331‐3p could be an independent prognostic marker for NSCLC patients. Furthermore, miR‐331‐3p significantly suppressed EMT, migration and metastasis of NSCLC cells in vitro and in vivo. Both ErbB2 and VAV2 were direct functional targets of miR‐331‐3p. The activities of Rac1, PAK1, and β‐catenin were regulated by miR‐331‐3p through ErbB2 and VAV2 targeting. These results indicated that miR‐331‐3p suppresses EMT, migratory capacity, and metastatic ability by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Zhu

Liu

et al. 2019

Cancer Science

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LINC00662 contributes to the progression and the radioresistance of cervical cancer by regulating miR‐497‐5p and CDC25A

Wei

Wang

Sun

et al. 2020

Cell Biochemistry & Function

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It is reported that long intergenic non-coding RNA 00662 (LINC00662) plays an oncogenic role in tumours. However, the mechanism of LINC00662 in regulating the progression and radiosensitivity of cervical cancer (CC) is not clear. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to detect LINC00662 and miR-497-5p expressions in CC tissues and cells. The expression of cell division cycle 25 A (CDC25A) in CC cells was examined by Western blot. CC cell proliferation was determined by cell counting kit-8 (CCK-8) and BrdU assays. The survival rate of CC cells was evaluated by colony formation assay under different doses of X-ray irradiation. CC cell migration and invasion were probed by Transwell assay. Besides, the interactions between miR-497-5p and LINC00662, and miR-497-5p and the 3 0 UTR of CDC25A were verified by dual-luciferase reporter assay, RIP assay, and RNA pull-down experiments. We demonstrated that, LINC00662 expression was remarkably raised in CC tissues and cell lines. LINC00662 overexpression promoted proliferation, migration, invasion and radioresistance of CC cells, and LINC00662 knockdown inhibited the above malignant phenotypes of CC cells. In terms of mechanism, LINC00662 facilitated CC progression and radioresistance by adsorbing miR-497-5p and indirectly up-regulating CDC25A expression. In a word, the LINC00662/miR-497-5p/CDC25A axis boosts proliferation and metastasis of CC cells and enhances the radioresistance of cancer cells. Significance of the study: CC poses a threat to the health of women all over the world. In this study, we demonstrated for the first time that LINC00662 expression was remarkably raised in CC tissues and cells. Cellular experiments confirmed that LINC00662 facilitated cell proliferation, migration, invasion and radiation resistance through the miR-497-5p/CDC25A axis, which might be a promising target for CC treatments.

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Long noncoding RNA HAGLR sponges miR‐338‐3p to promote 5‐Fu resistance in gastric cancer through targeting the LDHA‐glycolysis pathway

Huang

Ding³

et al. 2021

Cell Biology International

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Gastric cancer (GC) is one of the most common human malignancies due to its invasiveness and metastasis. 5-Fu is a widely applied chemotherapeutic agent against GC. Although 5-Fu therapy has achieved improvements in GC treatment, a large fraction of patients developed drug resistance which significantly limited its clinical applications. Recent studies revealed the pivotal roles of long noncoding RNAs (lncRNAs) in tumorigenesis and progressions of various tumors, including GC. However, the biological roles and molecular mechanisms of lncRNA HAGLR in GC remain unclear. Here, we report HAGLR was upregulated in both GC tissues and cell lines. In addition, HAGLR was associated with a poorly survival rate of GC patients. Blocking HAGLR inhibited GC cells proliferation and sensitized GC cells to 5-Fu. Bioinformatical analysis and luciferase assay demonstrated that HAGLR sponged microRNA (miR)-338-3p, which functions as a tumor suppressor in GC to downregulate its expressions. Moreover, from the established 5-Fu resistant GC cell line (HGC27 5-Fu R), we detected significantly elevated HAGLR, downregulated miR-338-3p, and glucose metabolism compared with parental HGC27 cells. We identified lactate dehydrogenase-A (LDHA), a glucose metabolism key enzyme, was the direct target of miR-338-3p in GC cells.Rescue experiments demonstrated that restoration of miR-338-3p in HAGLRoverexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Taken together, this study revealed essential roles and molecular mechanisms for the HAGLR-mediated 5-Fu resistance in GC, contributing to the development of new noncoding RNA-based therapeutic strategies against chemoresistant GC.

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LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

Cited by 166 publications

References 46 publications

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

LINC00662 contributes to the progression and the radioresistance of cervical cancer by regulating miR‐497‐5p and CDC25A

Long noncoding RNA HAGLR sponges miR‐338‐3p to promote 5‐Fu resistance in gastric cancer through targeting the LDHA‐glycolysis pathway

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