Long non‐coding small nucleolar RNA host genes in digestive cancers

Yang, Huan; Jiang, Zheng; Wang, Shuang; Zhao, Yongbing; Song, Xiaomei; Xiao, Yufeng; Yang, Shiming

doi:10.1002/cam4.2622

Cited by 56 publications

(57 citation statements)

References 112 publications

(283 reference statements)

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“…Dysregulation of the lncRNAs in bronchial epitheliums may contribute to the field cancerization in lung carcinogenesis. The SNHG family includes numerous members, whose dysregulations are associated with a variety of malignancies [53]. Each SNHG might contribute to tumorigenesis via multiple molecular regulatory mechanisms [53].…”

Section: Discussionmentioning

confidence: 99%

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A Non-Coding RNA Landscape of Bronchial Epitheliums of Lung Cancer Patients

et al. 2020

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We propose to systematically identify a non-coding RNA (ncRNA) profile of exfoliated bronchial epitheliums of sputum from lung cancer patients. Bronchial epithelial cells enriched from sputum of 32 lung cancer patients and 33 cancer-free smokers were analyzed by next-generation sequencing to comprehensively characterize the ncRNA profiles. In addition, 108 miRNAs, 88 small nucleolar RNAs, 13 piwi-interacting RNAs, 6 transfer RNAs, 4 ribosomal RNAs, 19 small nuclear RNAs, and 25 long-noncoding (lnc) RNAs displayed a significantly different level in bronchial epitheliums of sputum of lung cancer patients versus cancer-free smokers (all <0.001). PCR analysis confirmed their different expression levels in the sputum specimens. A high expression of SNHG9, an lncRNA, was validated in 78 lung tumor tissues, and the expression was inversely associated with overall survival of lung cancer patients (p = 0.002). Knockdown of SNHG9 in cancer cells reduced the cell growth, proliferation, and invasion in vitro and tumorigenesis in vivo. The multiple differentially expressed ncRNAs in bronchial epitheliums may contribute to the development and progression of lung cancer and provide potential biomarkers and therapeutic targets for the disease.

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Section: Discussionmentioning

confidence: 99%

“…The SNHG family includes numerous members, whose dysregulations are associated with a variety of malignancies [53]. Each SNHG might contribute to tumorigenesis via multiple molecular regulatory mechanisms [53]. For example, some SNHGs could act as sponges of microRNAs to inhibit the roles of miRNAs.…”

Section: Discussionmentioning

confidence: 99%

A Non-Coding RNA Landscape of Bronchial Epitheliums of Lung Cancer Patients

et al. 2020

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“…Small nucleolar RNA host gene 12 (SNHG12) is one of the classes of SNHGs [7]. Studies revealed that SNHG12 regulate cell proliferation, migration, invasion and metastasis in several cancers [8][9][10][11][12], indicating a potential target for cancer-directed interventions [13].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG12 promotes proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/ EIF5A

Liu

Che

et al. 2020

Preprint

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Background Although lncRNAs have reported to serve as potential biomarkers of atherosclerosis (AS), the role of lncRNA SNHG12 in AS are still unknown. Methods In present study, we investigated the regulatory effects of SNHG12 on human vascular smooth muscle cells (hVSMCs). RT-qPCR were employed to determine the expressions of SNHG12, miR-766-5p and eukaryotic translation initiation factor 5A (EIF5A). Cell viability was estimated via the Cell Counting Kit-8 assay. Wound healing and Transwell invasion assays were used for evaluation of hVSMCs migratory capacity. To further investigate the regulatory mechanisms, binding sites between SNHG12 and miR-766-5p, EIF5A and miR-766-5p were speculated via starBase V2.0, and validated using luciferase reporter gene assay. Results It was identified that SNHG12 was up-regulated in oxidized low-density lipoprotein (ox-LDL)-insulted hVSMCs. Silencing SNHG12 inhibited ox-LDL-induced proliferation and migration of hVSMCs. Moreover, we found that SNHG12 acted as a sponge of miR-766-5p, and miR-766-5p also interacted with EIF5A. EIF5A plasmids promoted the proliferation and migratory capacities of hVSMCs, however, shRNA-SNHG12 counteracted the facilitation of EIF5A plasmids on biological behaviors of hVSMCs. Conclusions These findings of this study demonstrated that SNHG12 facilitated the migration and invasion of hVSMCs via targeting miR-766-5p/EIF5A axis.

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“…Emerging evidences suggested that long non-coding RNAs (LncRNAs) controls tumorigenesis and development through regulating expressions of target genes (4)(5)(6). Importantly, a number of aberrant LncRNAs have been reported to be involved in cancer chemoresistance (7,8).…”

Section: Introductionmentioning

confidence: 99%

LncRNA BANCR Attenuates the Killing Capacity of Cisplatin on Gastric Cancer Cell through the ERK1/2 Pathway

Xiang

Liu

Fan

et al. 2020

Preprint

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Background Chemotherapy-based comprehensive treatment is the most important therapeutic method for patients with advanced gastric cancer, but chemoresistance often causes treatment failure. Long non-coding RNA (LncRNA) BRAF-activated non-coding RNA (BANCR) has been shown to participate in many biological behaviors of multiple cancers. However, the biological roles of LncRNA BANCR in chemoresistance of gastric cancer remain unclear. Here, we aimed to evaluate the functions of LncRNA BANCR in the therapy of gastric cancer. Methods In this study, LncRNA BANCR expression was detected in GC patient samples and cell lines by quantity polymerase chain reaction (qPCR). Cell proliferation and viability in cisplatin treated cells were measured using clonogenic survival assay and cell counting kit-8. The levels of ERK1/2 pathway molecules were tested with western blot. Ly3214996, an inhibitor of ERK signal pathway, administration was used to assess the effects of BANCR overexpression on GC cell cisplatin-treated resistance. Moreover, the role of BANCR in cisplatin resistance of GC was certified in xenograft mouse models in vivo. Results our study showed that LncRNA BANCR expression was also significantly increased in GC tissues compared with adjacent normal tissues. Furthermore, we found that BANCR overexpression promoted, while BANCR inhibited, GC cell resistance to cisplatin in vitro. Ly3214996 treatment abolished the BANCR overexpression-mediated GC cell cisplatin resistance via regulating the phosphorylation of ERK protein. Knock-down of BANCR delayed significantly tumor growth in xenograft mouse models. Conclusion BANCR promoted cisplatin resistance of GC cells by activating ERK1/2 pathway. Inhibition of BANCR was markedly suppressed the growth of gastric cancer cells in vitro as well as in vivo. This result provided a new strategy for gastric cancer via targeting BANCR

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Long non‐coding small nucleolar RNA host genes in digestive cancers

Cited by 56 publications

References 112 publications

A Non-Coding RNA Landscape of Bronchial Epitheliums of Lung Cancer Patients

A Non-Coding RNA Landscape of Bronchial Epitheliums of Lung Cancer Patients

LncRNA SNHG12 promotes proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/ EIF5A

LncRNA BANCR Attenuates the Killing Capacity of Cisplatin on Gastric Cancer Cell through the ERK1/2 Pathway

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