Risk SNP-induced lncRNA-SLCC1 drives colorectal cancer through activating glycolysis signaling

Yan, Tingting; Shen, Chaoqin; Jiang, Penglei; Yu, Chuangqi; Guo, Fangfang; Tian, Xianglong; Zhu, Xiaoqiang; Lu, Su; Han, Bingshe; Zhong, Ming; Chen, Jinxian; Liu, Qiang; Chen, Yingxuan; Zhang, Junfang; Hong, Jie; Chen, Haoyan; Fang, Jing‐Yuan

doi:10.1038/s41392-020-00446-7

Cited by 36 publications

(31 citation statements)

References 49 publications

(44 reference statements)

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“…Characterization of genetic variants with cancer development association can provide information on population risk stratification and prioritize the subgroups within a population for monitoring and primary prevention [338]. Combined with additional molecular biomarkers, determination of variant's involvement in a cancer-related phenotype can be used as a predictor for the patient's clinical outcome [339].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Non-Coding Variants in Cancer: Mechanistic Insights and Clinical Potential for Personalized Medicine

Lange

Begolli

Giakountis

2021

ncRNA

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The cancer genome is characterized by extensive variability, in the form of Single Nucleotide Polymorphisms (SNPs) or structural variations such as Copy Number Alterations (CNAs) across wider genomic areas. At the molecular level, most SNPs and/or CNAs reside in non-coding sequences, ultimately affecting the regulation of oncogenes and/or tumor-suppressors in a cancer-specific manner. Notably, inherited non-coding variants can predispose for cancer decades prior to disease onset. Furthermore, accumulation of additional non-coding driver mutations during progression of the disease, gives rise to genomic instability, acting as the driving force of neoplastic development and malignant evolution. Therefore, detection and characterization of such mutations can improve risk assessment for healthy carriers and expand the diagnostic and therapeutic toolbox for the patient. This review focuses on functional variants that reside in transcribed or not transcribed non-coding regions of the cancer genome and presents a collection of appropriate state-of-the-art methodologies to study them.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Non-Coding Variants in Cancer: Mechanistic Insights and Clinical Potential for Personalized Medicine

Lange

Begolli

Giakountis

2021

ncRNA

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“…LncRNA KCNQ1OT1 promotes CRC progression by increasing aerobic glycolysis through stabilizing HK2 [164]. In addition, LncRNA RAD51-AS1 and SLCC1 can all target HK2 [165,166].…”

Section: Epigenetics Direct Regulation Of Metabolism-related Genesmentioning

confidence: 99%

Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer

2021

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Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy.

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“…Notably, increasing number of lncRNAs have been linked to human diseases, including cancers [ 15 – 19 ]. For instance, upregulation of lncRNA SLCC1 promotes colorectal carcinogenesis through activating the glycolysis pathway [ 20 ]. Depletion of lncRNA XIST represses the progression of ovarian cancer cell by upregulating the expression of microRNA-149-3p [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes

Guo

et al. 2022

Mol Cancer

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Background Dysregulation of long noncoding RNAs (lncRNAs) has been linked to various human cancers. Bcr-Abl oncogene that results from a reciprocal translocation between human chromosome 9 and 22, is associated with several hematological malignancies. However, the role of lncRNAs in Bcr-Abl-induced leukemia remains largely unexplored. Methods LncRNA cDNA microarray was employed to identify key lncRNAs involved in Bcr-Abl-mediated cellular transformation. Abl-transformed cell survival and xenografted tumor growth in mice were evaluated to dissect the role of imatinib-upregulated lncRNA 1 (IUR1) in Abl-induced tumorigenesis. Primary bone marrow transformation and in vivo leukemia transplant using lncRNA-IUR1 knockout (KO) mice were further conducted to address the functional relevance of lncRNA-IUR1 in Abl-mediated leukemia. Transcriptome RNA-seq and Western blotting were performed to determine the mechanisms by which lncRNA-IUR1 regulates Bcr-Abl-induced tumorigenesis. Results We identified lncRNA-IUR1 as a critical negative regulator of Bcr-Abl-induced tumorigenesis. LncRNA-IUR1 expressed in a very low level in Bcr-Abl-positive cells from chronic myeloid leukemia patients. Interestingly, it was significantly induced in Abl-positive leukemic cells treated by imatinib. Depletion of lncRNA-IUR1 promoted survival of Abl-transformed human leukemic cells in experiments in vitro and xenografted tumor growth in mice, whereas ectopic expression of lncRNA-IUR1 sensitized the cells to apoptosis and suppressed tumor growth. In concert, silencing murine lncRNA-IUR1 in Abl-transformed cells accelerated cell survival and the development of leukemia in mice. Furthermore, lncRNA-IUR1 deficient mice were generated, and we observed that knockout of murine lncRNA-IUR1 facilitated Bcr-Abl-mediated primary bone marrow transformation. Moreover, animal leukemia model revealed that lncRNA-IUR1 deficiency promoted Abl-transformed cell survival and development of leukemia in mice. Mechanistically, we demonstrated that lncRNA-IUR1 suppressed Bcr-Abl-induced tumorigenesis through negatively regulating STAT5-mediated GATA3 expression. Conclusions These findings unveil an inhibitory role of lncRNA-IUR1 in Abl-mediated cellular transformation, and provide new insights into molecular mechanisms underlying Abl-induced leukemogenesis.

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Risk SNP-induced lncRNA-SLCC1 drives colorectal cancer through activating glycolysis signaling

Cited by 36 publications

References 49 publications

Non-Coding Variants in Cancer: Mechanistic Insights and Clinical Potential for Personalized Medicine

Non-Coding Variants in Cancer: Mechanistic Insights and Clinical Potential for Personalized Medicine

Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer

A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes

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