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long non-coding rna X-Inactive Specific Transcript Promotes Esophageal Squamous Cell Carcinoma Progression via the Microrna 34a/Zinc Finger E-box-Binding Homeobox 1 Pathway

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DIGESTIVE DISEASES AND SCIENCES 2024年第4期69卷 1169-1181页

作者： Guo, Bin He, Ming Ma, Minting Tian, Ziqiang Jin, Jing Tian, Guo Hebei Med Univ Hosp 4 Dept Thorac Surg 12 Jiankang Rd Shijiazhuang 050011 Hebei Peoples R China Hebei Med Univ Hosp 4 Dept Med Oncol 12 Jiankang Rd Shijiazhuang 050011 Hebei Peoples R China Hebei Med Univ Hosp 4 Dept Inst Canc 12 Jiankang Rd Shijiazhuang 050011 Hebei Peoples R China Hebei Med Univ Hosp 4 Dept Record Room 12 Jiankang Rd Shijiazhuang 050011 Hebei Peoples R China

BackgroundThe long non-coding rna X-inactive specific transcript (XIST) plays a crucial role in transcriptional silencing of the X chromosome. Zinc finger E-box-binding homeobox 1 (ZEB1) is a transcription factor involved in epithelial-mesenchymal transition (EMT) *** study aimed to investigate the impact of XIST on esophageal squamous cell carcinoma (ESCC) progression and its underlying mechanism involving the miR-34a/ZEB1/E-cadherin/EMT *** and ZEB1 expression were analyzed using quantitative PCR and immunohistochemistry. XIST knockdown was achieved in KYSE150 ESCC cells using sirna or shrna lentivirus transfection. Proliferation, migration, and invasion abilities were assessed, and luciferase reporter assays were performed to confirm XIST-miR-34a-ZEB1 interactions. In vivo ESCC growth was evaluated using a xenograft mouse *** and ZEB1 were upregulated in tumor tissues, correlating with metastasis and reduced survival. XIST knockdown inhibited proliferation, migration, and invasion of KYSE150 cells. It decreased ZEB1 expression, increased E-cadherin and miR-34a levels. Luciferase reporter assays confirmed miR-34a binding to XIST and ZEB1. XIST knockdown suppressed xenograft tumor *** promotes ESCC progression via the miR-34a/ZEB1/E-cadherin/EMT pathway. Targeting the XIST/miR-34a/ZEB1 axis holds therapeutic potential and serves as a prognostic biomarker in *** AbstractThis study has discovered an XIST-associated pathway involved in the regulation of ZEB1 expression, thereby influencing the progression of squamous cell carcinoma (ESCC). The specific mechanism is as follows: XIST can regulates ZEB1 expression by sponging miR-34a, ultimately promoting the metastasis of tumor by down-regulating the expression of E-cadherin.

关键词： Esophageal squamous cell carcinoma long non-coding rna X inactive specific transcript Zinc Finger E-box-Binding Homeobox 1 Microrna 34a Metastasis

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long non-coding rna GHET1 promotes gastric carcinoma cell proliferation by increasing c-Myc mrna stability

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FEBS JOUrnaL 2014年第3期281卷 802-813页

作者： Yang, Feng Xue, Xuchao Zheng, Luming Bi, Jianwei Zhou, Yuhong Zhi, Kangkang Gu, Yan Fang, Guoen Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Gen Surg Shanghai 200011 Peoples R China Second Mil Med Univ Changhai Hosp Dept Gen Surg Shanghai 200433 Peoples R China

long non-coding rnas (lncrnas), a recently characterized class of non-coding rnas, have been shown to have important regulatory roles and are de-regulated in a variety of tumors. However, the contributions of lncrnas to gastric carcinoma and their functional mechanisms remain largely unknown. In this study, we found that lncrna gastric carcinoma high expressed transcript 1 (lncrna-GHET1) was up-regulated in gastric carcinoma. The over-expression of this lncrna correlates with tumor size, tumor invasion and poor survival. Gain-of-function and loss-of-function analyses demonstrated that GHET1 over-expression promotes the proliferation of gastric carcinoma cells in vitro and in vivo. Knockdown of GHET1 inhibits the proliferation of gastric carcinoma cells. rna pull-down and immunoprecipitation assays confirmed that GHET1 physically associates with insulin-like growth factor 2 mrna binding protein 1 (IGF2BP1) and enhances the physical interaction between c-Myc mrna and IGF2BP1, consequently increasing the stability of c-Myc mrna and expression. The expression of GHET1 and c-Myc is strongly correlated in gastric carcinoma tissues. Depletion of c-Myc abolishes the effects of GHET1 on proliferation of gastric carcinoma cells. Taken together, these findings indicate that GHET1 plays a pivotal role in gastric carcinoma cell proliferation via increasing c-Myc mrna stability and expression, which suggests potential use of GHET1 for the prognosis and treatment of gastric carcinoma.

关键词： c-Myc gastric carcinoma insulin-like growth factor 2 mrna binding protein 1 long non-coding rna proliferation

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long non-coding rna RMST silencing protects against middle cerebral artery occlusion (MCAO)-induced ischemic stroke

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2018年第4期495卷 2602-2608页

作者： Hou, Xiao-Xia Cheng, Hong Nanjing Med Univ Affiliated Hosp 1 Dept Neurol Nanjing 210029 Jiangsu Peoples R China

long non-coding rnas (lncrnas) have emerged as major regulators in neurological diseases, and clarifying their roles in cerebral ischemic injury may provide novel targets for treating ischemic stroke. In this study, we mainly studied the role of lncrna-RMST in middle cerebral artery occlusion (MCAO)-induced mouse brain injury. We showed that RMST expression level was significantly up-regulated in oxygen-glucose deprivation (OGD)-treated primary hippocampal neuron, MCAO-induced injured brain, and the plasma of patients with ischemic stroke. RMST silencing protected against MCAO-induced ischemic brain injury in vivo and OGD-induced primary hippocampal neuron injury in vitro. Intra-cerebroventricular injection of RMST shrna significantly decreased brain RMST expression, reduced brain infarct size, and improved neurological function. Collectively, this study provides evidence that lncrna is involved in the pathogenesis of ischemic brain injury, and suggests a promising approach of RMST inhibition in treating ischemic stroke. (C) 2018 Elsevier Inc. All rights reserved.

关键词： long non-coding rna Ischemic stroke Middle cerebral artery occlusion

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long non-coding rna normalisers in human brain tissue

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JOUrnaL OF NEURAL TRANSMISSION 2015年第7期122卷 1045-1054页

作者： Kraus, Theo F. J. Greiner, Andrea Guibourt, Virginie Kretzschmar, Hans A. Univ Munich Ctr Neuropathol & Prion Res ZNP D-81377 Munich Bavaria Germany

The family of long non-coding rna (lncrna) is of increasing scientific interest as there is emerging evidence, that lncrnas are of essential importance for transcriptional and translational control, genomic imprinting and regulation of normal development as well as neuronal plasticity. As the generation of reliable expression profiles requires adequate normalisers, it is of fundamental importance to determine suitable references for lncrna studies. However, to date no systematic analysis of potential lncrna normalisers has been performed on human postmortem brain tissue samples. In this study, we investigated three different brain regions (cortex, white matter, and cerebellum) of human postmortem tissue and analysed the expression stability of 90 lncrnas. Bioinformatical analysis was performed to identify stably expressed lncrnas. Subsequently, lncrnas were classified according to their stability values using the NormFinder algorithm. We identified 30 suitable normalisers in cortex, 22 in white matter, and 41 in cerebellum. In addition, there were 13 suitable normalisers for studies comparing cortex and white matter, 25 for studies comparing cortex and cerebellum and 7 for studies comparing white matter and cerebellum. 5 lncrnas (LUST, IGF2AS (family), 7SK, HOXA6as, NDM29) showed stable expression in all investigated brain regions. A subsequent analysis of the influence of postmortem intervals (PMI) on expression of lncrnas revealed that expression levels of the newly identified 5 universal lncrna normalisers are stable within PMI of up to 27 h. Thus, these 5 lncrnas may be applicable as references for accurate normalisation of lncrna profiling in multiple brain regions during long PMI, enabling the generation of highly reproducible datasets in lncrna studies of the human brain.

关键词： long non-coding rna lncrna Normaliser References Postmortem stability Human brain tissue

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long non-coding rna Uc.187 Is Upregulated in Preeclampsia and Modulates Proliferation, Apoptosis, and Invasion of HTR-8/SVneo Trophoblast Cells

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JOUrnaL OF CELLULAR BIOCHEMISTRY 2017年第6期118卷 1462-1470页

作者： Cao, Chunyu Li, Jingyun Li, Jun Liu, Lan Cheng, Xiaoyan Jia, Ruizhe Maternal & Child Hlth Care Hosp Nantong Dept Obstet & Gynecol 399 Shiji Rd Nantong 226018 Jiangsu Peoples R China Nanjing Med Univ Dept Plast & Cosmet Surg State Key Lab Reprod Med Maternal & Child Hlth Med InstObstet & Gynecol H Nanjing 210004 Jiangsu Peoples R China Nanjing Med Univ Dept Obstet Obstet & Gynecol Hosp 123rd Tianfei StMochou Rd Nanjing 210004 Jiangsu Peoples R China

Among the preeclampsia-related long non-cording rnas (lncrnas) screened with a gene chip in our preliminary study, uc.187 attracted our attention because of its high conservation across different species and significant positive correlation with preeclampsia (PE). The literature and bioinformatics analysis suggested that lncrna uc. 187 might be associated with cell growth, invasion, and apoptosis. The expression of uc. 187 in severe preeclamptic placentas (n = 31) and normal placentas (n = 18) was evaluated by real-time reverse transcription polymerase chain reaction (qRT-PCR). We constructed a silencing lentivirus vector (uc. 187 sirna) to explore the biological function of uc. 187 in the development and progression of HTR-8/SVneo trophoblast cells in vitro. Furthermore, we utilized CCK8 analysis, a transwell invasion assay, and flow cytometry to determine the role of uc. 187 in the proliferation, invasion, and apoptosis of HTR-8/SVneo trophoblast cells. The proteins related to proliferation (PCNA, Ki67), invasion (MMP-2/-9 and TIMP-1), and apoptosis (caspase-3, Bcl-2) were evaluated with a Western blot assay. The results showed that there was an obvious upregulation of uc. 187 expression in preeclamptic placental tissues. In addition, uc. 187 silencing enhanced cell proliferation and invasion and reduced the cellular apoptotic response. Taken together, our findings suggest for the first time that abnormal expression of lncrna uc. 187 may lead to the aberrant biological behavior of HTR-8/SVneo cells. Therefore, we propose uc. 187 as a novel lncrna molecule that might contribute to the development of PE and might represent a potential diagnostic and therapeutic target for this disease. (C) 2016 Wiley Periodicals, Inc.

关键词： long non-coding rna lncrna UC 187 PROLIFERATION APOPTOSIS INVASION TROPHOBLAST CELLS

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long non-coding rna SOX21-AS1 sponges miR-145 to promote the tumorigenesis of colorectal cancer by targeting MYO6

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BIOMEDICINE & PHARMACOTHERAPY 2017年 96卷 953-959页

作者： Wei, An-Wei Li, Li-Fang Henan Univ Huaihe Hosp Dept Gastroenterol 8 Baogonghu North Rd Kaifeng 475000 Henan Peoples R China Henan Univ Huaihe Hosp Dept Gen Surg Kaifeng 475000 Henan Peoples R China

Emerging evidences have proved that long non-coding rnas (lncrnas) act as important molecular regulator in the tumor progression, including colorectal cancer (CRC). Lncrna SOX21-AS1 has been verified as oncogenic molecular in other cancers and tumorigenesis. In present study, our team investigates the clinical characteristic and molecular function in CRC carcinogenesis. Results showed that lncrna SOX21-AS1 expression was significantly over-expressed in CRC tissue samples and cells. The aberrant over-expression of SOX21-AS1 indicated poor prognosis of CRC patients. In vitro and in vivo validation experiments, SOX21-AS1 silencing inhibited the proliferation, invasion, and decreased the tumor growth of CRC cells. Moreover, miR-145 was proved to be the target of SOX21-AS1, besides, myosin VI (MYO6) was found to be one of the targets of miR-145 using bioinformatics prediction programs and rescue confirmation experiments. In summary, our study reveals the tumorigenic effect of lncrna SOX21-AS1 in CRC cells via targeting miR-145/MYO6, providing a novel insight for CRC carcinogenesis.

关键词： Colorectal cancer long non-coding rna SOX21-AS1 miR-145 MYO6

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long non-coding rna RP11-6O2.4 indicates poor prognosis and suppresses cell cycle progression through the p38-MAPK signaling pathway in gastric cancer

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MOLECULAR & CELLULAR TOXICOLOGY 2019年第3期15卷 335-344页

作者： Feng, Yang Fu, Zhiming Luo, Yajun Tan, Wang Liu, Zilin Ye, Pengcheng Lu, Fei Xiang, Wanping Tang, Linghan Yao, Lin Song, Mengyun Huang, Qingmei Liu, Yilun Xiao, Jiangwei Chengdu Univ Tradit Chinese Med Affiliated Hosp Coll Clin Med Chengdu Sichuan Peoples R China Hainan Gen Hosp Dept Gastrointestinal Surg Haikou Hainan Peoples R China Chengdu Med Coll Affiliated Hosp 1 Dept Gastrointestinal Surg Chengdu Sichuan Peoples R China North Sichuan Med Coll Affiliated Hosp Dept Gastrointestinal Surg Nanchong Sichuan Peoples R China North Sichuan Med Coll Affiliated Hosp Dept Gastroenterol Nanchong Sichuan Peoples R China North Sichuan Med Coll Affiliated Hosp Dept Oncol Nanchong Sichuan Peoples R China Chengdu Med Coll Affiliated Hosp 1 Dept Burn Surg Chengdu Sichuan Peoples R China Chongqing Med Univ Affiliated Hosp 1 Chongqing Peoples R China

Backgrounds: The role of long non-coding rnas (lncrna) in gastric cancer (GC) has been highlighted in studies conducted over the past decade. However, the potential clinical value and the mechanisms of action of RP11-6O2.4 in GC have not been thoroughly elucidated to date. The specific aim of the present study was to assess RP11-6O2.4 and to explore its role in human ***: Quantitative real-time polymerase chain reaction (qPCR) was performed to analyze the expression levels of RP11-6O2.4 in GC tissues, paired adjacent noncancerous tissues (ANTs) and GC cell lines. In addition, the correlation between RP11-6O2.4 expression and the clinical characteristics and prognosis of patients with GC was statistically analyzed. The effects of RP11-6O2.4 on the GC cell cycle transformation through the p38-MAPK signaling pathway were explored by flow cytometry, qPCR and Western blot analysis after treatment with SB203580, a p38MAPK specific inhibitor, in ***: The expression levels of RP11-6O2.4 in GC tissues were significantly lower than the paired ANTs (P<0.05). In addition, RP11-6O2.4 expression was significantly lower in cases with older age, longer maximum tumor diameter, higher ASA grade and deeper invasive depth (P<0.05). RP11-6O2.4 expression was significantly higher in cases with well/middle differentiation than poor/no differentiation;higher in cases without lymph node metastasis than in lymph node metastasis;and higher in cases in stage I/II than in stage III/IV. An in vitro assay showed that RP11-6O2.4 induced G0/G1 phase cell cycle arrest, likely by regulating the p38-MAPK signaling ***: The above mentioned data suggested that RP11-6O2.4 was a tumor-suppressor gene in GC. RP11-6O2.4 might play an important role in the cell cycle transformation by regulating the p38-MAPK signaling pathway, thereby representing a specific biomarker and a potential molecular target for the treatment of GC.

关键词： long non-coding rna Gastric cancer RP11-6O2.4 p38-MAPK

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long non-coding rna PANDAR correlates with poor prognosis and promotes tumorigenesis in hepatocellular carcinoma

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BIOMEDICINE & PHARMACOTHERAPY 2015年 72卷 113-118页

作者： Peng, Wei Fan, Hong Nanjing Med Univ Jiangsu Canc Hosp Dept Med Oncol Nanjing 210009 Jiangsu Peoples R China First Peoples Hosp Yunnan Prov Dept Digest Dis Kunming Peoples R China

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide. long non-coding rnas (lncrnas) are new-found non-coding rnas longer than 200 nucleotides, and have emerged as important players in tumorigenesis. However, the clinical significance and molecular mechanism of lncrnas in HCC remain largely elusive. The aim of this study was to determine the expression pattern and clinical value of PANDAR, a novel lncrna, in HCC. qRT-PCR was conducted in tissues and cell lines. Then, associations between PANDAR expression and clinicopathological features of HCC patients were further analyzed. Next, ROC curve was constructed to evaluate diagnostic values. Finally, effects of PANDAR on HCC cell phenotypes were verified. PANDAR was overexpressed in HCC tissues and cell lines. Moreover, its expression level was significantly correlated with liver cirrhosis, HBsAg, AFP, tumor nodule, vascular invasion and TNM stage. PANDAR overexpression was associated with poorer survival and shorter recurrence. Importantly, the area under the ROC curve of PANDAR was up to 0.9564. Furthermore, PANDAR knockdown significantly repressed cell proliferation, colony formation and cycle progression of HCC in vitro. PANDAR was a powerful tumor biomarker, which highlighted its potential clinical utility as a promising prognostic biomarker and therapeutic target. (C) 2015 Elsevier Masson SAS. All rights reserved.

关键词： Hepatocellular carcinoma long non-coding rna PANDAR Biomarker Prognosis

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long non-coding rna MALAT-1 modulates metastatic potential of tongue squamous cell carcinomas partially through the regulation of small proline rich proteins

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BMC CANCER 2016年第1-Sup期16卷 1-10页

作者： Fang, Zhengyu Zhang, Shanshan Wang, Yufan Shen, Shiyue Wang, Feng Hao, Yinghua Li, Yuxia Zhang, Bingyue Zhou, You Yang, Hongyu Shenzhen Peking Univ Biomed Res Inst Hong Kong Univ Sci & Technol Med Ctr Shenzhen Guangdong Peoples R China Peking Univ Shenzhen Hosp Dept Oral & Maxillofacial Shenzhen Guangdong Peoples R China

Background: We previously described several abnormally expressed long non-coding rna (lncrna) in tong squamous cell carcinomas (TSCCs) that might be associated with tumor progression. In the present study, we aimed to investigate the role of abnormally expressed metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) lncrna in the metastatic potential of TSCC cells and its molecular mechanisms. Methods: Expression levels of MALAT-1 lncrna were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in 127 TSCC samples as well as paired adjacent normal tissues and lymph node metastases (if exist). Lentiviral vectors expressing short hairpin rna (shrna) were used to knock down the expression of MALAT1 gene in two TSCC cell lines (CAL27 and SCC-25) with relatively higher MALAT-1 expression. Proliferational ability of the TSCC cells was analyzed using water soluble tetrazolium-1 (WST-1) assay. Metastatic abilities of TSCC cells were estimated in-vitro and in-vivo. We also performed a microarray-based screen to identify the genes influenced by MALAT-1 alteration, which were validated by real-time PCR analysis. Results: Expression of MALAT-1 lncrna was enhanced in TSCCs, especially in those with lymph node metastasis (LNM). Knockdown (KD) of MALAT-1 lncrna in TSCC cells led to impaired migration and proliferation ability in-vitro and fewer metastases in-vivo. DNA microarray analysis showed that several members of small proline rich proteins (SPRR) were up-regulated by KD of MALAT-1 lncrna in TSCC cells. SPRR2A over-expression could impair distant metastasis of TSCC cells in-vivo. Conclusion: Enhanced expression of MALAT-1 is associated with the growth and metastatic potential of TSCCs. Knock down of MALAT-1 in TSCCs leads to the up-regulation of certain SPRR proteins, which influenced the distant metastasis of TSCC cells.

关键词： Tongue squamous cell cancer long non-coding rna MALAT-1 Cancer metastasis

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long non-coding rna and rna-binding protein interactions in cancer: Experimental and machine learning approaches

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SEMINARS IN CANCER BIOLOGY 2022年第Part3期86卷 325-345页

作者： Shaath, Hibah Vishnubalaji, Radhakrishnan Elango, Ramesh Kardousha, Ahmed Islam, Zeyaul Qureshi, Rizwan Alam, Tanvir Kolatkar, Prasanna R. Alajez, Nehad M. Hamad Bin Khalifa Univ HBKU Qatar Biomed Res Inst QBRI Qatar Fdn QF Translat Canc & Immun Ctr TCIC POB 34110 Doha Qatar Hamad Bin Khalifa Univ HBKU Qatar Fdn QF Coll Hlth & Life Sci POB 34110 Doha Qatar Hamad Bin Khalifa Univ HBKU Qatar Biomed Res Inst QBRI Qatar Fdn Diabet Res Ctr DRC POB 34110 Doha Qatar Hamad Bin Khalifa Univ HBKU Qatar Fdn Coll Sci & Engn POB 34110 Doha Qatar

Understanding the complex and specific roles played by non-coding rnas (ncrnas), which comprise the bulk of the genome, is important for understanding virtually every hallmark of cancer. This large group of molecules plays pivotal roles in key regulatory mechanisms in various cellular processes. Regulatory mechanisms, mediated by long non-coding rna (lncrna) and rna-binding protein (RBP) interactions, are well documented in several types of cancer. Their effects are enabled through networks affecting lncrna and RBP stability, rna metabolism including N-6-methyladenosine (m(6)A) and alternative splicing, subcellular localization, and numerous other mechanisms involved in cancer. In this review, we discuss the reciprocal interplay between lncrnas and RBPs and their involvement in epigenetic regulation via histone modifications, as well as their key role in resistance to cancer therapy. Other aspects of RBPs including their structural domains, provide a deeper knowledge on how lncrnas and RBPs interact and exert their biological functions. In addition, current state-of-the-art knowledge, facilitated by machine and deep learning approaches, unravels such interactions in better details to further enhance our understanding of the field, and the potential to harness rna-based therapeutics as an alternative treatment modality for cancer are discussed.

关键词： long non-coding rna Lncrna, rna-binding protein RBP, lncrna-protein interaction (LPI) Cancer Mechanisms of action Structural and functional domains Machine learning Deep learning

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