Regulatory mechanisms of long noncoding RNAs on gene expression in cancers

Sun, Weiliang; Yang, Yingzhen; Xu, Cai; Guo, Junming

doi:10.1016/j.cancergen.2017.06.003

Cited by 174 publications

(131 citation statements)

References 56 publications

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“…Thus, it is important to elucidate the roles and mechanisms involved in ox-LDLinduced cellular progression. Despite their original definition of "transcriptional noise," lncRNAs play roles multiple biological processes, including chromatin dynamics, cell growth, cell proliferation, cell apoptosis, cell differentiation, cell metastasis, the cell cycle and tumorigenesis via the modulation of gene expression at the transcriptional, posttranscriptional and translational levels (Quinn and Chang, 2016;Sun et al, 2017). Despite their original definition of "transcriptional noise," lncRNAs play roles multiple biological processes, including chromatin dynamics, cell growth, cell proliferation, cell apoptosis, cell differentiation, cell metastasis, the cell cycle and tumorigenesis via the modulation of gene expression at the transcriptional, posttranscriptional and translational levels (Quinn and Chang, 2016;Sun et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Silencing of MEG3 inhibited ox‐LDL‐induced inflammation and apoptosis in macrophages via modulation of the MEG3/miR‐204/CDKN2A regulatory axis

Long

Liu

Yin

et al. 2019

Cell Biology International

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Atherosclerosis (AS) is one of the most common chronic inflammatory diseases and a major cause of morbidity and mortality. However, the underlying molecular mechanisms of the progression of AS are still largely unknown. Increasing evidence has demonstrated that long noncoding RNAs (lncRNAs) play important roles in a variety of biological processes and the physiological and pathological progression of human diseases. In this study, we aimed to explore the role and underlying molecular mechanism of lncRNA MEG3 in Raw264.7 cells treated with oxidized low-density lipoprotein (ox-LDL). First, we found that ox-LDL inhibited the cell viability and proliferation, increased TNFa and IL1b secretion and induced the apoptosis of Raw264.7 cells. Second, we demonstrated that ox-LDL upregulated MEG3 expression and that knockdown of MEG3 inhibited the action of ox-LDL in Raw264.7 cells. Third, we showed that MEG3 sponged miR-204 in Raw264.7 cells treated with ox-LDL. Fourth, we demonstrated that miR-204 regulated the expression of cyclin-dependent kinase inhibitor 2A (CDKN2A) in Raw264.7 cells treated with ox-LDL. Finally, we revealed that MEG3 exerted its function via the regulation of the MEG3/miR-204/CDKN2A regulatory axis in Raw264.7 cells treated with ox-LDL. In summary, our study identified the role of the MEG3/miR-204/CDKN2A pathway in Raw264.7 cells treated with ox-LDL, revealed a novel regulatory pathway in AS and indicated potential novel characteristic biomarkers and therapeutic targets for AS.

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Section: Introductionmentioning

confidence: 99%

Silencing of MEG3 inhibited ox‐LDL‐induced inflammation and apoptosis in macrophages via modulation of the MEG3/miR‐204/CDKN2A regulatory axis

Long

Liu

Yin

et al. 2019

Cell Biology International

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“…21,22 Recent studies have shown that MALAT1 played important role in regulating multiple pathophysiological processes in vascular diseases, neurologic disorders and cancers, including migration, proliferation, invasion and apoptosis. 21,22 Recent studies have shown that MALAT1 played important role in regulating multiple pathophysiological processes in vascular diseases, neurologic disorders and cancers, including migration, proliferation, invasion and apoptosis.…”

mentioning

confidence: 99%

MALAT1 promoted cell proliferation and migration via MALAT1/miR‐155/MEF2A pathway in hypoxia of cardiac stem cells

Wang

Chen

2018

J of Cellular Biochemistry

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Accumulating evidence revealed that hypoxia contributed to many human diseases, including ischemic myocardium and heart failure (HF). In recent years, the roles of hypoxia in stem cell survival and cardiac biology have been studied extensively. However, the underlying molecular mechanisms remain to be elucidated. As a leading cause of HF, ischemic heart disease was correlated with hypoxia. In this study, we firstly constructed the hypoxia cell model by CoCl2 in cardiac stem cells (CSCs) and found that hypoxia induced the cell proliferation and migration potential in CSCs. Then, we demonstrated that the expression of metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) was promoted in CoCl2‐induced CSCs hypoxia model. Furthermore, we found that knockdown of MALAT1 inhibited the cell proliferation and migration in CoCl2‐induced CSCs hypoxia model. In addition, we revealed that MALAT1 regulated the microRNA‐155 (miR‐155) expression in CSCs under both the normal and hypoxia conditions and further, manipulation of the miR‐155 expression affected the role of MALAT1 in CoCl2‐induced CSCs hypoxia cell model. We then illustrated that miR‐155 regulated the myocyte enhancer factor 2A (MEF2A) expression in CSCs under both the normal and hypoxia conditions and further, changing the expression of MEF2A affected the role of miR‐155. Finally, we demonstrated that MALAT1 regulated the MEF2A expression and exerted its role via modulation of the MALAT1/miR‐155/MEF2A pathway. Taken together, our study illustrated that MALAT1 promoted the cell proliferation and migration in CoCl2‐induced CSCs hypoxia model, acting mechanistically by promoting MEF2A expression via “sponging” miR‐155.

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“…Studies in our laboratory also demonstrated that rs2151280 in noncoding ANRIL RNA gene (antisense noncoding RNA in proximity to the INK4‐ARF locus, also designated as CDKN2BAS ) was significantly associated with PFS in the same cohort of MM patients . ANRIL is able to transcriptionally repress the transcription of the entire INK4‐ARF locus (including p15 , p14ARF , and p16 tumor suppressor genes), thus simultaneously modulating both the p53 and pRb pathways, both of which are directly/indirectly involved in DNA repair, apoptosis, and other cellular processes . Our further analyses showed that ANRIL rs2151280, XRCC1 rs25487, and the risk level appeared to be three independent predictive factors of PFS in this patient cohort (Table , Multivariate model II).…”

Section: Resultsmentioning

confidence: 69%

XRCC1‐mediated DNA repair is associated with progression‐free survival of multiple myeloma patients after autologous stem cell transplant

Persaud

Johnson

Seligson

et al. 2019

Molecular Carcinogenesis

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Autologous stem cell transplant (ASCT) with high‐dose melphalan (HDM) is the standard treatment for fit multiple myeloma (MM) patients. It is generally believed that some DNA repair proteins impact the activity to repair melphalan‐induced DNA damage, thus potentially contributing to the patient's clinical response. However, knowledge of these proteins is limited. In the current study, we investigated the roles of XRCC1, a protein involved in base excision repair and single‐strand break repair, in melphalan response in MM cells. Small interfering RNA knockdown of XRCC1 significantly increased the accumulation of melphalan‐induced DNA damage in MM cells and sensitized them to melphalan treatment, indicating that genetic variation in XRCC1 may impact response to melphalan treatment. We then evaluated the association between an XRCC1 variant with reduced activity, rs25487 (R399Q), and clinical outcomes of 108 MM patients with melphalan therapy. Our results showed that XRCC1 rs25487 was associated with prolonged progression‐free survival (PFS) in MM patients. The adjusted hazard ratio for PFS between patients carrying rs25487 AA/AG and GG was 0.42 (95% confidence interval: 0.25, 0.84, P = .014). Taken together, these results indicate that XRCC1 is involved in the repair of melphalan‐induced DNA damage and XRCC1 rs25487 variant with impaired DNA repair function influences the clinical responses of HDM in MM patients.

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Regulatory mechanisms of long noncoding RNAs on gene expression in cancers

Cited by 174 publications

References 56 publications

Silencing of MEG3 inhibited ox‐LDL‐induced inflammation and apoptosis in macrophages via modulation of the MEG3/miR‐204/CDKN2A regulatory axis

Silencing of MEG3 inhibited ox‐LDL‐induced inflammation and apoptosis in macrophages via modulation of the MEG3/miR‐204/CDKN2A regulatory axis

MALAT1 promoted cell proliferation and migration via MALAT1/miR‐155/MEF2A pathway in hypoxia of cardiac stem cells

XRCC1‐mediated DNA repair is associated with progression‐free survival of multiple myeloma patients after autologous stem cell transplant

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