KIF9‑AS1, LINC01272 and DIO3OS lncRNAs as novel biomarkers for inflammatory bowel disease

Wang, Sen; Hou, Yong; Chen, Weiping; Wang, Jianmin; Xie, Weihua; Zhang, Xiaoping; Zeng, Li

doi:10.3892/mmr.2017.8118

Cited by 42 publications

(50 citation statements)

References 35 publications

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“…LINC01272 has been shown to be associated with a myeloid proinflammatory signature in Crohn's disease and was significantly upregulated in inflammatory bowel disease. 38,39 Moreover, LINC01272 is closely related to the survival time of lung squamous cell carcinoma. 40 Nevertheless, the target genes are unidentified and the mechanism remains unclear.…”

Section: Discussionmentioning

confidence: 99%

<p>LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT</p>

Leng¹,

Liu²,

Wang³

et al. 2020

OTT

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Purpose: Gastric cancer (GC) is the fifth most common tumor in the world, and most patients with GC have a poor prognosis. This study aimed to explore the biological influence and mechanism of LINC01272 in GC. Materials and Methods: Using bioinformatic analyses, we investigated the expression of LINC01272 in TCGA database and predicted the biological functions and mechanism of LINC01272 in GC. Then, we detected the expression of LINC01272 in GC cell lines, GC tissues, and corresponding normal tissues using real-time polymerase chain reaction (RT-PCR). Finally, we explored the migration and invasion ability of LINC01272 by wound-healing and Transwell assays and examined the expression of epithelial-mesenchymal transition (EMT)related proteins through Western blotting. Results: We found that LINC01272 was upregulated in GC and was associated with GC staging and lymph node metastasis. The results of wound-healing and Transwell assays revealed that the LINC01272 was closely related to GC cell migration and invasion. LINC01272 knockdown inhibited the migration and invasion ability of GC cells by reducing the expression of EMT-related proteins. Overexpression of LINC01272 had the opposite effect. Conclusion: Together, our results showed that LINC01272 promoted GC metastasis ability by regulating the expression of EMT-related proteins and could serve as a potential diagnostic biomarker for GC.

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Section: Discussionmentioning

confidence: 99%

<p>LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT</p>

Leng¹,

Liu²,

Wang³

et al. 2020

OTT

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“…Therefore, determining the involvement of cancer-specific lncRNAs may prove beneficial for identifying novel targets for anticancer treatment. Wang et al ( 11 ) suggested that lncRNA KIF9-AS1 may belong to a novel group of non-coding RNAs, which are associated with inflammation and tumorigenesis ( 12 ). Thus, the present study aimed to determine the expression levels of KIF9-AS1 in NPC tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, lncRNA PICART1 was reported to inhibit the progression of non-small cell lung cancer cells through inactivation of the AKT1 signaling pathway ( 10 ), and lncRNA XIST is associated with a poor prognosis and promotes a malignant phenotype in osteosarcoma ( 11 ). Recently, KIF9-AS1 was also reported to be a biomarker for inflammatory bowel disease ( 12 ). However, to the best of our knowledge, there are currently no relevant studies regarding the role of KIF9-AS1 in NPC.…”

Section: Introductionmentioning

confidence: 99%

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

You

Wang

2020

Oncol Lett

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Long non-coding RNAs (lncRNAs) have been reported to serve a crucial role in the progression of nasopharyngeal carcinoma (NPC); however, the underlying molecular mechanisms of lncRNA KIF9-AS1 in the tumorigenesis of NPC remains poorly understood. Reverse transcription-quantitative PCR was used to analyze the expression levels of KIF9-AS1 and microRNA (miR)-16, and Cell Counting Kit-8, wound healing and Transwell assays were used to determine the cell viability, invasion and migration, respectively, of NPC cells. In addition, a dual-luciferase reporter assay was used to analyze the direct interaction between KIF9-AS1 and miR-16. NPC stage was classified according to the seventh edition of the AJCC staging system. The results revealed that KIF9-AS1 expression levels were upregulated in NPC tissues and cell lines. In addition, miR-16 was demonstrated to directly interact with KIF9-AS1 and inhibit KIF9-AS1 expression levels, whereas the miR-16 inhibitor rescued the effects of the KIF9-AS1-knockdown in NPC cells. Furthermore, the expression levels of KIF9-AS1 were upregulated, while those of miR-16 were downregulated in NPC tissues. Notably, the expression levels of KIF9-AS1 were observed to be significantly more upregulated in advanced tumors (III–IV vs. I–II) and patients with high KIF9-AS1 expression levels exhibited a worse prognosis. In conclusion, the findings of the present study suggested that KIF9-AS1 may promote the progression of NPC by targeting miR-16, thus KIF9-AS1 may be a novel molecular target for NPC therapy.

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“…Likewise, a few other studies have analyzed smaller datasets and observed changes in IBD speci c ncRNAs, i.e. LINC01272 10 , DIO3OS 11 , and KIF9-AS 11 using RT-PCR in intestinal tissues and plasma samples in IBD. In particular, the expression of these ncRNAs was greater in IBD patients when compared to controls 11 .…”

Section: Introductionmentioning

confidence: 99%

“…LINC01272 10 , DIO3OS 11 , and KIF9-AS 11 using RT-PCR in intestinal tissues and plasma samples in IBD. In particular, the expression of these ncRNAs was greater in IBD patients when compared to controls 11 . However, none of these studies explored whether the ncRNAs expression are speci c to tissue types, CD disease behaviors, disease location or disease in ammation.…”

Section: Introductionmentioning

confidence: 99%

Profiling Non-Coding RNA Levels With Clinical Classifiers in Pediatric Crohn’s Disease

Pelia

Venkateswaran

Matthews

et al. 2020

Preprint

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Background: Crohn’s disease (CD) is a heritable chronic inflammatory disorder. Non-coding RNAs (ncRNAs) play an important role in epigenetic regulation by affecting gene expression, but can also directly affect protein function, thus having a substantial impact on biological processes. We investigated whether non-coding RNAs (ncRNA) at diagnosis are dysregulated during CD at different CD locations and future disease behaviors to determine if ncRNA signatures can serve as an index to outcomes. Methods: Using subjects belonging to the RISK cohort, we analyzed ncRNA from the ileal biopsies of 345 CD and 71 non-IBD controls, and ncRNA from rectal biopsies of 329 CD and 61 non-IBD controls. Sequence alignment was done (STAR package) using Human Genome version 38 (hg38) as reference panel. The differential expression (DE) analysis was performed with EdgeR package and DE ncRNAs were identified with a threshold of fold change (FC) >2 and FDR < 0.05 after multiple test corrections. Results: In total, we identified 130 CD specific DE ncRNAs (89 in ileum and 41 in rectum) when compared to non-IBD controls. Similarly, 35 DE ncRNAs were identified between B1 and B2 in ileum, whereas no differences among CD disease behaviors were noticed in rectum. We also found inflammation specific ncRNAs between inflamed and non-inflamed groups in ileal biopsies. Overall, we observed that expression of mir1244-2, mir1244-3, mir1244-4, and RN7SL2 were increased during CD, regardless of disease behavior, location, or inflammatory status. Lastly, we tested ncRNA expression at baseline as potential tool to predict the disease status, disease behaviors and disease inflammation at 3-year follow up.Conclusions: We have identified ncRNAs that are specific to disease location, disease behavior, and disease inflammation in CD. Both ileal and rectal specific ncRNA are changing over the course of CD, specifically during the disease progression in the intestinal mucosa. Collectively, our findings show changes in ncRNA during CD and may have a clinical utility in early identification and characterization of disease progression.

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KIF9‑AS1, LINC01272 and DIO3OS lncRNAs as novel biomarkers for inflammatory bowel disease

Cited by 42 publications

References 35 publications

<p>LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT</p>

<p>LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT</p>

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

Profiling Non-Coding RNA Levels With Clinical Classifiers in Pediatric Crohn’s Disease

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