&lt;p&gt;LncRNA TMPO-AS1 Promotes Proliferation and Invasion by Sponging miR-383-5p in Glioma Cells&lt;/p&gt;

Liu, Guoyuan; Yang, Haiying; Cao, Lei; Han, Ke; Li, Guobin

doi:10.2147/cmar.s282539

Cited by 11 publications

(5 citation statements)

References 19 publications

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“…In the TMPO-AS1/miR-383-5p pathway, miR-383-5p functions as a direct target of lncRNA TMPO antisense RNA1 (TMPO-AS1). In glioma cells, overexpression of TMPO-AS1 together with the low expression of miR-383-5p has been linked with proliferation and migration ( Liu et al, 2020 ). Inhibition of TMPO-AS1 and increased expression of miR-383-5p inhibited glioma progression.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-383: A tumor suppressor miRNA in human cancer

Jafarzadeh

Noori

Sarrafzadeh

et al. 2022

Front. Cell Dev. Biol.

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Downregulated expression of anti-tumor miR-383 has been found in many kinds of cancer. MiR-383 family members can directly target the 3′-untranslated region (3′-UTR) of the mRNA of some pro-tumor genes to attenuate several cancer-related processes, including cell proliferation, invasion, migration, angiogenesis, immunosuppression, epithelial-mesenchymal transition, glycolysis, chemoresistance, and the development of cancer stem cells, whilst promoting apoptosis. Functionally, miR-383 operates as a tumor inhibitor miRNA in many types of cancer, including breast cancer, hepatocellular carcinoma, gastric cancer, pancreatic cancer, colorectal cancer, esophageal cancer, lung cancer, head and neck cancer, glioma, medulloblastoma, melanoma, prostate cancer, cervical cancer, oral squamous cell carcinoma, thyroid cancer, and B-cell lymphoma. Both pro-tumor and anti-tumor effects have been attributed to miR-383 in ovarian cancer. However, only the pro-tumor effects of miR-383 were reported in cholangiocarcinoma. The restoration of miR-383 expression could be considered a possible treatment for cancer. This review discusses the anti-tumor effects of miR-383 in human cancers, emphasizing their downstream target genes and potential treatment approaches.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-383: A tumor suppressor miRNA in human cancer

Jafarzadeh

Noori

Sarrafzadeh

et al. 2022

Front. Cell Dev. Biol.

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“…Conversely, the lncRNAs identified in this study could act as drivers of chemoresistance in sarcomas through their sponging role regarding miRNAs ( Figure 4 ). In agreement with this, accumulating evidence suggests that LOXL1-AS1 [ 66 , 67 , 68 , 69 ], HAGLR [ 70 , 71 ], LINC00997 [ 72 ], and TMPO-AS1 [ 73 , 74 , 75 ] contribute to carcinogenesis by acting as molecular sponges of miRNAs.…”

Section: Resultsmentioning

confidence: 67%

Soft Tissue Ewing Sarcoma Cell Drug Resistance Revisited: A Systems Biology Approach

Asfa

Toy

Bonab

et al. 2023

IJERPH

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Ewing sarcoma is a rare type of cancer that develops in the bones and soft tissues. Drug therapy represents an extensively used modality for the treatment of sarcomas. However, cancer cells tend to develop resistance to antineoplastic agents, thereby posing a major barrier in treatment effectiveness. Thus, there is a need to uncover the molecular mechanisms underlying chemoresistance in sarcomas and, hence, to enhance the anticancer treatment outcome. In this study, a differential gene expression analysis was conducted on high-throughput transcriptomic data of chemoresistant versus chemoresponsive Ewing sarcoma cells. By applying functional enrichment analysis and protein–protein interactions on the differentially expressed genes and their corresponding products, we uncovered genes with a hub role in drug resistance. Granted that non-coding RNA epigenetic regulators play a pivotal role in chemotherapy by targeting genes associated with drug response, we investigated the non-coding RNA molecules that potentially regulate the expression of the detected chemoresistance genes. Of particular importance, some chemoresistance-relevant genes were associated with the autonomic nervous system, suggesting the involvement of the latter in the drug response. The findings of this study could be taken into consideration in the clinical setting for the accurate assessment of drug response in sarcoma patients and the application of tailored therapeutic strategies.

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“…TMPO has been shown to induce proliferation and inducing cell cycle arrest and apoptosis in glioblastoma ( 75 ). Thus, unsurprisingly, the knockdown of TMPO-AS1 suppressed growth and increased apoptosis in thyroid cancer ( 76 ), glioma progression ( 77 ), and cell proliferation and motility in pancreatic carcinoma ( 72 ). Moreover, reduced expression of TMPO-AS1 increased overall survival and impaired growth of esophageal squamous cell carcinoma tumors ( 73 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of lncRNAs involved in response to ionizing radiation in fibroblasts of long-term survivors of childhood cancer and cancer-free controls

et al. 2023

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IntroductionLong non-coding ribonucleic acids (lncRNAs) are involved in the cellular damage response following exposure to ionizing radiation as applied in radiotherapy. However, the role of lncRNAs in radiation response concerning intrinsic susceptibility to late effects of radiation exposure has not been examined in general or in long-term survivors of childhood cancer with and without potentially radiotherapy-related second primary cancers, in particular.MethodsPrimary skin fibroblasts (n=52 each) of long-term childhood cancer survivors with a first primary cancer only (N1), at least one second primary neoplasm (N2+), as well as tumor-free controls (N0) from the KiKme case-control study were matched by sex, age, and additionally by year of diagnosis and entity of the first primary cancer. Fibroblasts were exposed to 0.05 and 2 Gray (Gy) X-rays. Differentially expressed lncRNAs were identified with and without interaction terms for donor group and dose. Weighted co-expression networks of lncRNA and mRNA were constructed using WGCNA. Resulting gene sets (modules) were correlated to the radiation doses and analyzed for biological function.ResultsAfter irradiation with 0.05Gy, few lncRNAs were differentially expressed (N0: AC004801.4; N1: PCCA-DT, AF129075.3, LINC00691, AL158206.1; N2+: LINC02315). In reaction to 2 Gy, the number of differentially expressed lncRNAs was higher (N0: 152, N1: 169, N2+: 146). After 2 Gy, AL109976.1 and AL158206.1 were prominently upregulated in all donor groups. The co-expression analysis identified two modules containing lncRNAs that were associated with 2 Gy (module1: 102 mRNAs and 4 lncRNAs: AL158206.1, AL109976.1, AC092171.5, TYMSOS, associated with p53-mediated reaction to DNA damage; module2: 390 mRNAs, 7 lncRNAs: AC004943.2, AC012073.1, AC026401.3, AC092718.4, MIR31HG, STXBP5-AS1, TMPO-AS1, associated with cell cycle regulation).DiscussionFor the first time, we identified the lncRNAs AL158206.1 and AL109976.1 as involved in the radiation response in primary fibroblasts by differential expression analysis. The co-expression analysis revealed a role of these lncRNAs in the DNA damage response and cell cycle regulation post-IR. These transcripts may be targets in cancer therapy against radiosensitivity, as well as provide grounds for the identification of at-risk patients for immediate adverse reactions in healthy tissues. With this work we deliver a broad basis and new leads for the examination of lncRNAs in the radiation response.

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<p>LncRNA TMPO-AS1 Promotes Proliferation and Invasion by Sponging miR-383-5p in Glioma Cells</p>

Cited by 11 publications

References 19 publications

MicroRNA-383: A tumor suppressor miRNA in human cancer

MicroRNA-383: A tumor suppressor miRNA in human cancer

Soft Tissue Ewing Sarcoma Cell Drug Resistance Revisited: A Systems Biology Approach

Identification of lncRNAs involved in response to ionizing radiation in fibroblasts of long-term survivors of childhood cancer and cancer-free controls

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