Helicobacter pylori infection, H19 and LINC00152 expression in serum and risk of gastric cancer in a Chinese population

Yang, Tian; Zeng, Hongmei; Chen, Wanqing; Zheng, Rongshou; Zhang, Yang; Li, Zhexuan; Qi, Jun; Wang, Minjie; Chen, Tianhui; Lou, Jianlin; Lu, Lingeng; Zhou, Tong; Dai, Shuyang; Meng, Chao; You, Wei‐Cheng; Pan, Kai-Feng

doi:10.1016/j.canep.2016.08.015

Cited by 63 publications

(50 citation statements)

References 39 publications

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“…Our former study revealed that LINC00152 promoted tumor invasion and predicts poor prognosis in renal clear cell [8] and lung carcinomas [9] . Other studies have got similar findings in gastric cancer [10] and hepatic carcinoma [11] , suggesting that LINC00152 might serve as a powerful oncogenic lncRNA in somatic malignancies. Researchers have found that LINC00152 forms the loop feedback with FOXM1 to stimulate tumor growth [12] and might serve as the ceRNA (competing endogenous RNA) to regulate miRNAs to fulfil its biological functions [5,13,14] .…”

Section: Introductionsupporting

confidence: 59%

LINC00152 promotes Ovarian tumor progression and Predicts Poor Prognosis by inhibiting the ubiquitination of BCL6

Wang

Weng

Chen

et al. 2020

Preprint

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Background : Long non-coding RNA 00152 (LINC00152) has been found oncogenic in multiple somatic malignancies. But its roles in the ovarian cancer remain elusive. We aim to investigate its functions and mechanism in the ovarian tumor progression.Methods: We used RNAscope and RT-qPCR assays to detect the LINC00152 levels in 152 pairs of ovarian tumor and paratumorous tissues, conducted in vitro and in vivo experiments to evaluate its biological functions, and performed RNA immunoprecipitation, RNA-pulldown, MS/LS analysis, mutant construction and ubiquitination assays to explore the LINC00152-BCL6 binding and regulation.Results: LINC00152 was abnormally increased in the ovarian tumor tissues and its high expression predicted poorer survivals of patients; overexpression of LINC00152 promoted ovarian tumor proliferation and metastasis both in vitro and in vivo ; LINC00152 bond to Serine333 and Serine343 of BCL6 and then suppressed its ubiquitination; Finally, LINC00152 facilitated its oncogenic functions in a BCL6-mediated manner in ovarian cancer.Conclusions: LINC00152 is the independent prognostic predictor of ovarian cancer; and the abnormal expression of LINC00152 facilitates ovarian tumor proliferation and invasion by suppress the ubiquitination of BCL6. Our data might be helpful in exploring the molecular mechanisms of lncRNAprotein interactions, and might provide the potential target for the tumor pharmacology of ovarian cancer.

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Section: Introductionsupporting

confidence: 59%

LINC00152 promotes Ovarian tumor progression and Predicts Poor Prognosis by inhibiting the ubiquitination of BCL6

Wang

Weng

Chen

et al. 2020

Preprint

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“…LINC00152 was overexpressed in several cancers, including esophageal squamous cell carcinoma, colorectal cancer, gastric cancer, and hepatocellular carcinoma . Increased LINC00152 levels might be potential biomarkers for predicting the poor progress of these cancers . Mechanistically, LINC00152 overexpression dramatically promoted gallbladder cancer growth by regulating the phosphatidylinositol 3‐kinase (PI3K)/AKT signaling pathway .…”

Section: Discussionmentioning

confidence: 99%

“…25 Increased LINC00152 levels might be potential biomarkers for predicting the poor progress of these cancers. [26][27][28][29][30][31] Mechanistically, LINC00152 overexpression dramatically promoted gallbladder cancer growth by regulating the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. 9 Chen et al revealed that LINC00152 was dramatically upregulated in gastric cancer and was positively correlated with tumor invasion, TNM stage, and poor survival.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR‐125b with MCL‐1 by regulating mitochondrial apoptosis pathways in ovarian cancer

et al. 2018

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Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia‐1 (MCL‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC00152, while MCL‐1 was positively related to the LINC00152 level. MiR‐125b could affect LINC00152 levels as evaluated by qRT‐PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL‐1 expression and MCL‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR‐125b. In summary, based on ceRNA theory, the combined research on miR‐125b and MCL‐1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.

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“…Lastly, linc00152 is upregulated in various cancers including gastric cancer [145,147,352,353], lung cancer [144], gall bladder cancer [148,149], renal cell carcinoma [354], and pancreatic cancer [355], whilst its expression has been found to be downregulated in colorectal cancer [356]. linc00152 can act via a ceRNA network for miR-139-5p in gastric cancer [143], and acts as a competing endogenous RNA to modulate the expression of miR-193a-3p in colon cancer [151], and acts as a ceRNA for miR-138 in gallbladder cancer [148].…”

Section: Lncrnas and Emt: The Main Playersmentioning

confidence: 99%

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Heery

Finn

Cuffe

et al. 2017

Cancers

163

140

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Epithelial mesenchymal transition (EMT), the adoption by epithelial cells of a mesenchymal-like phenotype, is a process co-opted by carcinoma cells in order to initiate invasion and metastasis. In addition, it is becoming clear that is instrumental to both the development of drug resistance by tumour cells and in the generation and maintenance of cancer stem cells. EMT is thus a pivotal process during tumour progression and poses a major barrier to the successful treatment of cancer. Non-coding RNAs (ncRNA) often utilize epigenetic programs to regulate both gene expression and chromatin structure. One type of ncRNA, called long non-coding RNAs (lncRNAs), has become increasingly recognized as being both highly dysregulated in cancer and to play a variety of different roles in tumourigenesis. Indeed, over the last few years, lncRNAs have rapidly emerged as key regulators of EMT in cancer. In this review, we discuss the lncRNAs that have been associated with the EMT process in cancer and the variety of molecular mechanisms and signalling pathways through which they regulate EMT, and finally discuss how these EMT-regulating lncRNAs impact on both anti-cancer drug resistance and the cancer stem cell phenotype.

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Helicobacter pylori infection, H19 and LINC00152 expression in serum and risk of gastric cancer in a Chinese population

Cited by 63 publications

References 39 publications

LINC00152 promotes Ovarian tumor progression and Predicts Poor Prognosis by inhibiting the ubiquitination of BCL6

LINC00152 promotes Ovarian tumor progression and Predicts Poor Prognosis by inhibiting the ubiquitination of BCL6

Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR‐125b with MCL‐1 by regulating mitochondrial apoptosis pathways in ovarian cancer

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

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