lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Cao, Feng; Wang, Zhiguo; Feng, Yong; Zhu, Hongjun; Yang, Mei-ju; Zhang, Shuanglin; Wang, Xuefeng

doi:10.3892/or.2020.7522

Cited by 22 publications

(21 citation statements)

References 53 publications

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“…The results of the present study confirmed that mirna-106a-5p serves as an oncogene by augmenting TPTeP1-mediated stemness and radioresistance of glioma. Previous studies have demonstrated the stimulating effects of TPTeP1 and the inhibitory effect of mirna-106a-5p on cancer cell apoptosis (33,35,43). Thus, prospective studies will aim to elucidate the effect of TPTeP1 and mir-106-5p on glioma cell apoptosis.…”

Section: Discussionmentioning

confidence: 98%

“…TPTeP1 acts as a tumor suppressor in hepatocellular carcinoma (33,34) and lung cancer (35), and has been reported to participate in the modulation of several biological functions, including cell proliferation, invasion, chemoresistance and inflammation (33)(34)(35) . In addition, bioinformatic analysis suggests that TPTeP1 may serve as a tumor suppressor in the development of GBM (36).…”

Section: Discussionmentioning

confidence: 99%

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lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR‑106a‑5p‑mediated P38 MAPK signaling

et al. 2020

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Glioma is diagnosed as the most common intracranial malignant tumor. cancer stem cells determine stemness and radioresistance, and may facilitate glioma recurrence. The present study aimed to investigate whether the long non-coding rna (lncrna) transmembrane phosphatase with tensin homology pseudogene 1 (TPTeP1) regulated cell stemness and radioresistance of glioma, and determine the underlying molecular mechanism of TPTeP1 in the modulation of glioma progression. cell and molecular biology techniques were applied for investigating the role of TPTeP1 in glioma cell lines, animal model, and clinical samples. The results demonstrated that TPTeP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo. in addition, TPTeP1 augmented MaPK14 expression by competitively interacting with microrna (mir)-106a-5p, thus activating the P38 MaPK signaling pathway, and suppressing glioma stemness and radioresistance. TPTeP1 functionally bound to mir-106a-5p, which formed a reciprocal regulatory loop to stimulate the P38 MaPK signaling pathway. low TPTeP1 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues, and were positively associated with poor prognosis of patients with glioma. Furthermore, analysis using data from The cancer Genome atlas database confirmed the molecular mechanism and biological significance of dysregulation of TPTEP1 in glioma progression. Taken together, the results of the present study suggest that TPTeP1 may be applied as a diagnostic and prognostic indicator for glioma, and may be an alternative target for the treatment of glioma.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR‑106a‑5p‑mediated P38 MAPK signaling

et al. 2020

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“…Several aberrantly expressed lncRNAs have been found associated with B–ALL [ 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ]. For instance, Fernando et al [ 19 ] highlighted the over–expression of the lncRNA CASC15 with regulatory roles on the transcriptional factor SOX4, in paediatric RUNX–1 translocated B–ALL.…”

Section: Introductionmentioning

confidence: 99%

lncRNAs–mRNAs Co–Expression Network Underlying Childhood B–Cell Acute Lymphoblastic Leukaemia: A Pilot Study

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Pane

Smaldone

et al. 2020

Cancers

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Long non–coding RNAs (lncRNAs) are emerging as key gene regulators in the pathogenesis and development of various cancers including B lymphoblastic leukaemia (B–ALL). In this pilot study, we used RNA–Seq transcriptomic data for identifying novel lncRNA–mRNA cooperative pairs involved in childhood B–ALL pathogenesis. We conceived a bioinformatic pipeline based on unsupervised PCA feature extraction approach and stringent statistical criteria to extract potential childhood B–ALL lncRNA signatures. We then constructed a co–expression network of the aberrantly expressed lncRNAs (30) and protein–coding genes (754). We cross–validated our in–silico findings on an independent dataset and assessed the expression levels of the most differentially expressed lncRNAs and their co–expressed mRNAs through ex vivo experiments. Using the guilt–by–association approach, we predicted lncRNA functions based on their perfectly co–expressed mRNAs (Spearman’s correlation) that resulted closely disease–associated. We shed light on 24 key lncRNAs and their co–expressed mRNAs which may play an important role in B–ALL pathogenesis. Our results may be of clinical utility for diagnostic and/or prognostic purposes in paediatric B–ALL management.

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“…As reported before, various lncRNAs can regulate cell proliferation and migration. For instance, lncRNA TPTEP1 could inhibit the non-small cell lung cancer (NSCLC) cells to proliferate through abating miR-328-5p expression (Cao et al, 2020). In addition, in renal cell carcinoma, lncRNA00312 attenuated cell proliferation and migration obviously (Zeng et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

lncRNA-RMST functioned as a SOX2 transcription co-regulator to regulate miR-1251 in the progression of Hirschsprung’s disease

Zhou¹,

Zhi²,

Chen³

et al. 2020

Preprint

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Hirschsprung’s disease (HSCR) is a congenital disorder characterized by the absence of enteric neural crest cells (ENCCs). Non-coding RNAs including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been authenticated as important regulators of biological functions. We conducted a microarray analysis and found lncRNA Rhabdomyosarcoma 2-associated transcript (RMST) was down-regulated in the stenotic segment of HSCR patients. MiR-1251 is transcribed from the intron region of RMST and was also low-expressed. When the expression of RMST or miR-1251 was reduced, the cell proliferation and migration were attenuated. However, RMST didn’t affect the expression of miR-1251 directly found in this study. Through bioinformatic analysis, transcription factor SOX2 was predicted to bind to the promoter region of miR-1251 which was confirmed by CHIP assay. Herein, we demonstrated that RMST exerted as a co-regulator of SOX2 to regulate the expression of miR-1251. Furtherly, AHNAK was proved to be the target gene of miR-1251 in this study. Taken together, we revealed the role of RMST/SOX2/miR-1251/AHNAK pathway in the occurrence of Hirschsprung’s disease and provided a potential therapeutic target for this disease.SUMMARY STATEMENTHirschsprung disease (HSCR) is characterized by a deficit in enteric neurons, however, the underlying mechanism remains unclear. This study revealed the role of lnc-RMST during the occurrence of HSCR.

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lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Cited by 22 publications

References 53 publications

lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR‑106a‑5p‑mediated P38 MAPK signaling

lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR‑106a‑5p‑mediated P38 MAPK signaling

lncRNAs–mRNAs Co–Expression Network Underlying Childhood B–Cell Acute Lymphoblastic Leukaemia: A Pilot Study

lncRNA-RMST functioned as a SOX2 transcription co-regulator to regulate miR-1251 in the progression of Hirschsprung’s disease

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