LncRNA MIR155HG Promotes Temozolomide Resistance by Activating the Wnt/β-Catenin Pathway Via Binding to PTBP1 in Glioma

He, Xin; Sheng, Jie; Yu, Wei; Wang, Kejian; Zhu, Shaojun; Liu, Qian

doi:10.1007/s10571-020-00898-z

Cited by 28 publications

(25 citation statements)

References 56 publications

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“…Knockdown of lnc00462717 increases the accumulation of doxorubicin (Dox) in glioma via interacting with PTBP1 to inhibit the miR-5p/Occludin signaling pathway [20]. Furthermore, PTBP1, mediated by lncRNA MIR155HG, could upregulate the activation of Wnt/β-catenin signaling pathway in TMZ resistance to glioma has been demonstrated in our previous research [21]. Up to date, the activation of Wnt/β-catenin pathway occurs widely in in glioma chemoresistance to TMZ [22,23].…”

Section: Introductionmentioning

confidence: 81%

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LncRNA GAS5 Inhibits Temozolomide Chemoresistance to Glioma Via Inactivating Wnt/β-Catenin Pathway by Interacting with PTBP1

Sheng

Chen

et al. 2021

Preprint

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Purpose Temozolomide-based therapeutic resistance has become the crucial cause of chemotherapy failure in glioma treatment. Long non-coding RNA (lncRNA) growth arrest-specific 5 (GAS5) is reported to be downregulated in glioma and to inhibit tumor progression and metastasis. This study aimed to investigate function and potential regulatory mechanism of GAS5 in temozolomide (TMZ) chemoresistance to glioma.Methods qRT-PCR, western blotting and immunofluorescence were used to measure the levels of GAS5 and proteins. RNA-binding protein immunoprecipitation assay was used to analyze the interaction between GAS5 and PTBP1. Flow cytometry apoptosis assay, CCK-8 assay, colony formation assay and nude mice xenograft experiments were used to detect the effects of GAS5 on TMZ resistance in glioma.Results Downregulation of GAS5 might predict a poor prognosis in glioma patients. Overexpression of GAS5 improves the sensitivity to TMZ in glioma cells. Mechanistically, GAS5 could interact with polypyrimidine tract binding protein 1 (PTBP1) to downregulate its expression, thereby inactivating the Wnt/β-catenin pathway. Moreover, GAS5 could increase the anti-tumor effect of TMZ in vivo. Conclusion This study indicated that GAS5 contributed to TMZ chemoresistance of glioma through interacting with PTBP1, and then inhibiting Wnt/β-catenin pathway, which provides a novel approach to develop promising therapeutic strategy.

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Section: Introductionmentioning

confidence: 81%

“…According to our pervious study, the half maximal inhibitory concentrations (IC50s) of TMZ in A172 and U251 cells were 1200 µM and 150 µM, respectively [21]. Based on this result, the transfected U251 and A172 cells were treated with TMZ at IC50 doses for another 72h.…”

Section: Flow Cytometry Apoptosis Assaymentioning

confidence: 92%

LncRNA GAS5 Inhibits Temozolomide Chemoresistance to Glioma Via Inactivating Wnt/β-Catenin Pathway by Interacting with PTBP1

Sheng

Chen

et al. 2021

Preprint

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“…Above all, the present study suggested that miR155HG expression may be associated with OC development. Previous studies have demonstrated that miR155HG participates in the malignant biological behavior of diverse cancers (24,32,33). miR155HG silencing diminishes cell viability while facilitating cell apoptosis by targeting PTBP1 to restrain glioma development (32).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that miR155HG participates in the malignant biological behavior of diverse cancers (24,32,33). miR155HG silencing diminishes cell viability while facilitating cell apoptosis by targeting PTBP1 to restrain glioma development (32). miR155HG knockdown upregulates miR-155-3p and downregulates TP53INP1, thus retarding the biological behavior of non-small cell lung cancer (33).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA miR155HG silencing restrains ovarian cancer progression by targeting the microRNA‑155‑5p/tyrosinase‑related protein 1 axis

Wen

Luo

et al. 2021

Exp Ther Med

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Ovarian cancer (OC) is the third commonest gynecological malignancy worldwide. The long non-coding (lnc)RNA microRNA (miR)155HG functions as an oncogene in different human cancers. However, the function and molecular mechanism of miR155HG in OC remain elusive. The present study indicated that the expression levels of miR155HG and tyrosinase-related protein 1 (TYRP1) were significantly increased, whereas that of miR155-5p was decreased in OC tissues and cells, as detected by real-time quantitative polymerase chain reaction. It was demonstrated that knockdown of miR155HG markedly inhibited OC cell viability, migration and invasion while promoting apoptosis, as indicated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, Transwell and western blot assays. Mechanistically, it was revealed that miR155HG and TYRP1 were both targeted by miR-155-5p with complementary binding sites in the 3' untranslated region. A dual-luciferase reporter assay was used to confirm the targeting relationship between miR155HG, miR-155-5p and TYRP1. In addition, the interaction between miR155HG and miR-155-5p was further demonstrated by radioimmunoprecipitation and pull-down assays. In addition, feedback approaches determined that miR-155-5p inhibition or TYRP1 overexpression markedly reversed the inhibitory effects of miR155HG knockdown on OC cell viability, migration and invasion as well as weakened the promotive effect of miR155HG knockdown on OC cell apoptosis. Thus, miR155HG silencing inhibited the malignant biological behavior of OC cells by targeting the miR-155-5p/TYRP1 axis. The present study provides novel insights into the underlying mechanism of OC progression.

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“…NEAT1 and FoxD2-AS1 hypermethylated of the promoter region of MGMT, hence mediate temozolomide resistance [133,134]. LncRNA MIR155HG induced temozolomide resistance in glioma cells through targeting and activating the Wnt/β-catenin pathway [124]. LncRNA SOX2OT was involved in the development of MDR against temozolomide in glioblastoma cells through upregulating SOX2 expression, which activated the Wnt5a/β-catenin signaling pathway (Figure 4) [125].…”

Section: Nck1-as1 Upregulatedmentioning

confidence: 99%

Long Non-Coding RNAs in Multidrug Resistance of Glioblastoma

Mahinfar

Baradaran

Davoudian

et al. 2021

Genes

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Glioblastoma, also known as glioblastoma multiforme, is the most aggressive brain tumor in adults. Despite the huge advance in developing novel therapeutic strategies for patients with glioblastoma, the appearance of multidrug resistance (MDR) against the common chemotherapeutic agents, including temozolomide, is considered as one of the important causes for the failure of glioblastoma treatment. On the other hand, recent studies have demonstrated the critical roles of long non-coding RNAs (lncRNAs), particularly in the development of MDR in glioblastoma. Therefore, this article aimed to review lncRNA’s contribution to the regulation of MDR and elucidate the underlying mechanisms in glioblastoma, which will open up new lines of inquiry in the treatment of glioblastoma.

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LncRNA MIR155HG Promotes Temozolomide Resistance by Activating the Wnt/β-Catenin Pathway Via Binding to PTBP1 in Glioma

Cited by 28 publications

References 56 publications

LncRNA GAS5 Inhibits Temozolomide Chemoresistance to Glioma Via Inactivating Wnt/β-Catenin Pathway by Interacting with PTBP1

LncRNA GAS5 Inhibits Temozolomide Chemoresistance to Glioma Via Inactivating Wnt/β-Catenin Pathway by Interacting with PTBP1

Long non‑coding RNA miR155HG silencing restrains ovarian cancer progression by targeting the microRNA‑155‑5p/tyrosinase‑related protein 1 axis

Long Non-Coding RNAs in Multidrug Resistance of Glioblastoma

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