RETRACTED ARTICLE: Long non-coding RNA MACC1-AS1 promoted pancreatic carcinoma progression through activation of PAX8/NOTCH1 signaling pathway

Chen, Qi; Chen, Xiaofeng; Li, Dongen; Yang, Lifen; Xu, Liping; Y, Hu; Jianshuai, Jiang

doi:10.1186/s13046-019-1332-7

Cited by 49 publications

(40 citation statements)

References 20 publications

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“…4 lncRNAs act as signaling molecules, scaffolds, and instructors, and exert their influence at several levels including transcription, post-transcription, and translation. 5 In recent years, abundant evidence has revealed that anomalous expression of lncRNAs such as HOXD-AS1, H19, CASC9, and NORAD [6][7][8][9] may drive the pathogenesis of breast cancer. In addition, anomalous expression of lncRNAs may serve as a biomarker for breast cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

Yan

Zhang

Yin

et al. 2020

OTT

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To investigate the association between the lncRNA NEAT1 and breast cancer, and to determine the influence of NEAT1 on regulation of other signaling molecules in breast cancer. Methods: In the present study, we measured levels of the lncRNA NEAT1 in 106 breast cancer patients and in a human breast cancer cell line by qRT-PCR. The correlation between NEAT1 expression and patients' clinical characteristics was analyzed with in-house and TCGA data. We used cellular functioning assays and cell immunofluorescence assay to evaluate the role of NEAT1 and its target molecules in proliferation, invasion and migration in breast cancer. We used Western blotting to explore possible targets of NEAT1 and a subcellular fractionation assay to locate NEAT1 expression. Results: NEAT1 was overexpressed in breast cancer tissue and also closely related to advanced clinical stages and positive lymph node metastases. NEAT1 levels were also tightly correlated to prognosis for breast cancer patients in survival analyses. Cellular function assays revealed that downregulation of NEAT1 could inhibit breast cancer cell viability, invasion and migration. Western blotting revealed down-regulation of CBX7 and upregulation of RTCB following NEAT1 inhibition. Based on the cytoplasmic and nuclear expression of NEAT1, we investigated the possible regulation of CBX7 and RTCB by NEAT1. Results showed that NEAT1 regulated the expression of CBX7 and RTCB, possibly by binding of NEAT1 to DNA in the nucleus, which facilitates cell proliferation, invasion and migration. Conclusion: The current results suggest that the lncRNA NEAT1 is upregulated in breast cancer and facilitates tumor cell viability, invasion and migration via CBX7 and RTCB.

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Section: Introductionmentioning

confidence: 99%

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

Yan

Zhang

Yin

et al. 2020

OTT

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“…Higher expression of lncRNA MACC1-AS1 correlates with the lung metastasis of gastric cancer cells, and MACC1-AS1 is elevated under metabolic stress and facilitates metabolic plasticity by increasing MACC1 mRNA expression and strengthening glycolysis and anti-oxidative abilities via the AMPK/Lin28 pathway (121). LncRNA MACC1-AS1 is also upregulated in pancreatic cancer and related to poor prognosis, and its knockdown inhibits the metastasis of pancreatic cancer cells by upregulating the expression of PAX8 (paired-box gene 8), which plays a role in activating NOTCH1 signaling and promoting cell aerobic glycolysis (122).…”

Section: Lkb1-amp Activated Protein Kinase Pathwaymentioning

confidence: 99%

Non-Coding RNAs Operate in the Crosstalk Between Cancer Metabolic Reprogramming and Metastasis

Sun

2020

Front. Oncol.

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Metastasis, the spread of cancer cells from a primary tumor to a secondary site, represents one of the hallmarks of malignancies and the leading cause of cancer-related death. The process of metastasis is a result of the interaction of genetic heterogeneity, abnormal metabolism, and tumor microenvironments. On the other hand, metabolic reprogramming, another malignancy hallmark, refers to the ability of cancer cells to alter metabolic and nutrient acquisition modes in order to support the energy demands for accomplishing the rapid growth, dissemination, and colonization. Cancer cells remodel metabolic patterns to supplement nutrients for their metastasis and also undergo metabolic adjustments at different stages of metastasis. Genes and signaling pathways involved in tumor metabolic reprogramming crosstalk with those participating in metastasis. Non-coding RNAs are a group of RNA molecules that do not code proteins but have pivotal biological functions. Some of microRNAs and lncRNAs, which are the two most extensively studied non-coding RNAs, have been identified to participate in regulating metabolic remodeling of glucose, lipid, glutamine, oxidative phosphorylation, and mitochondrial respiration, as well as the process of metastasis involving cell motility, transit in the circulation and growth at a new site. This article reviews recent progress on non-coding RNAs operating in the crosstalk between tumor metabolic reprogramming and metastasis, particularly those influencing metastasis through regulating metabolism, and the underlying mechanisms of how they exert their regulatory functions.

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“…Among these, long non-coding RNAs (lncRNAs), which are over 200 nucleotides in length, have emerged as key regulators in biological processes for their diverse and complex work mechanisms [4]. LncRNAs have been reported to affect an array of cellular functions, such as cellular growth, apoptosis, migration and invasion, as well as EMT progression [5][6][7][8]. Also, increasing lncRNAs have been detected to be aberrantly expressed in cancers.…”

Section: Introductionmentioning

confidence: 99%

Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

Rong

Wang

et al. 2020

J Exp Clin Cancer Res

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Background: Revealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet. Materials and methods: qRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes. Results: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop. Conclusion: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.

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RETRACTED ARTICLE: Long non-coding RNA MACC1-AS1 promoted pancreatic carcinoma progression through activation of PAX8/NOTCH1 signaling pathway

Cited by 49 publications

References 20 publications

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

Non-Coding RNAs Operate in the Crosstalk Between Cancer Metabolic Reprogramming and Metastasis

Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

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