LNC00673 suppresses proliferation and metastasis of pancreatic cancer via target miR-504/ HNF1A

Gong, Yi; Dai, Hai-Su; Shu, Jun-Jie; Liu, Wei; Bie, Ping; Zhang, Leida

doi:10.7150/jca.32855

Cited by 22 publications

(22 citation statements)

References 27 publications

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“…LINC00673 expression was found to be significantly reduced in PC cells, where it functions to suppress cell invasion and migration by inhibiting miR-504 (ref. 18 ). In addition, the lncRNA PXN-AS1 was identified as a ceRNA for miR-3064 and, through miR-3064 sequestration, was found to promote the expression of the tumor suppressor PIP4K2B, resulting in the inhibition on PC progression 19 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

Wang

et al. 2021

Cell Death Dis

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An accumulation of evidence indicates that long noncoding RNAs are involved in the tumorigenesis and progression of pancreatic cancer (PC). In this study, we investigated the functions and molecular mechanism of action of LINC00941 in PC. Quantitative PCR was used to examine the expression of LINC00941 and miR-335-5p in PC tissues and cell lines, and to investigate the correlation between LINC00941 expression and clinicopathological features. Plasmid vectors or lentiviruses were used to manipulate the expression of LINC00941, miR-335-5p, and ROCK1 in PC cell lines. Gain or loss-of-function assays and mechanistic assays were employed to verify the roles of LINC00941, miR-335-5p, and ROCK1 in PC cell growth and metastasis, both in vivo and in vitro. LINC00941 and ROCK1 were found to be highly expressed in PC, while miR-335-5p exhibited low expression. High LINC00941 expression was strongly associated with larger tumor size, lymph node metastasis, and poor prognosis. Functional experiments revealed that LINC00941 silencing significantly suppressed PC cell growth, metastasis and epithelial–mesenchymal transition. LINC00941 functioned as a molecular sponge for miR-335-5p, and a competitive endogenous RNA (ceRNA) for ROCK1, promoting ROCK1 upregulation, and LIMK1/Cofilin-1 pathway activation. Our observations lead us to conclude that LINC00941 functions as an oncogene in PC progression, behaving as a ceRNA for miR-335-5p binding. LINC00941 may therefore have potential utility as a diagnostic and treatment target in this disease.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

Wang

et al. 2021

Cell Death Dis

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“…Additionally, LINC00673 is also correlated with good outcomes in PDAC patients. It can negatively regulate miR-504 to inhibit the progression of PDAC (73). There are many potential lncRNAs biomarkers that remain to be explored and translated to clinical practices.…”

Section: Meg3mentioning

confidence: 99%

Non-coding RNAs in Pancreatic Ductal Adenocarcinoma

Gong

Jiang

2020

Front. Oncol.

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“…Currently, LncRNAs act as quenchers of miRNA to regulate tumor progress 26 . For example, the proliferative, invasiveness, and migratory capacity of pancreatic cancer cell lines are regulated by LncRNA linc00673 by sequestering miR-504 27 . Previous study indicated that EIF3J-AS1 may induce HCC progression via sponging miR-122e-5p 15 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

Wei

Wang

Liang

et al. 2020

Sci Rep

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Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients. Esophageal cancer (ECa) is of particularly high incidence in Chinese males compared to other regions and remains a global threat to human health. Up to ~ 450,000 new cases of ECa are diagnosed annually, of which up to ~ 400,000 of those afflicted do not survive 1. Diagnostic and therapeutic advances have been made to improve ECa therapeutics, including biopsies, chromo endoscopy and narrow-band imaging 2. However, despite these improvements, the efficiency of ECa therapies and subsequent patient prognosis remains poor. ECa therefore remains a global health burden for which new diagnostics and effective therapeutic strategies are urgently required 3. A further understanding of the molecular regulators of ECa tumorigenesis is required to expedite the discovery of novel anti-ECa strategies. While lncRNAs (long noncoding RNAs; more than 200 bases long 4-8 are not capable of translating proteins, their dysregulation is observed several cancers, such as ECa 9-12. For instance, the process of EMT (epithelialmesenchymal transition) is enhanced by lncRNA PVT1 via E-cadherin suppression in ECa 13. Further, significantly enhanced level of CASC11 was observed in ECa tissues while its silencing impeded the progression of ECa by regulating KLF6 expression 14. Previous study reported that up-regulated a novelty EIF3J-AS1 was associated with poor survival and accelerated HCC progression via targeting miR-122e5p/CTNND2 axis under hypoxia 15. Meanwhile, EIF3J-AS1 induced by H3K27 promoted colorectal cancer proliferation and inhibited apoptosis via miR-3163/YAP1 axis 16. Nevertheless, the role and inherent mechanisms of EIF3J-AS1 in human ECa development remains to be assessed. In this research, we examined the increased expression of EIF3J-AS1 in ECa cell lines and tissues, the effect of EIF3J-AS1 knocked down on inhibiting the metastasis and growth of ECa cell lines in vitro and vivo. We also examined the role of EIF3J-AS1 in ECa cells' aggressive phenotypes by miR-373-3p binding and assessing the AKT1 expression. Materials and methods Tissue specimens. Collection of a total of 182 ECa cases...

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LNC00673 suppresses proliferation and metastasis of pancreatic cancer via target miR-504/ HNF1A

Cited by 22 publications

References 27 publications

Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

Non-coding RNAs in Pancreatic Ductal Adenocarcinoma

LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

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