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pmid:37202742

LncRNA-PVT1 was identified as a key regulator for TMZ resistance and STAT-related pathway in glioma.

Yusheng Chen · Fengjin Ma · Zhe Zhang · Yang Guo · Hanwei Shen · Hang Chen

BMC cancer · 2023 doi:10.1186/s12885-023-10937-9

Paper

complete

Experiment

partial

Data

partial

Analysis

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title
LncRNA-PVT1 was identified as a key regulator for TMZ resistance and STAT-related pathway in glioma.
doi
10.1186/s12885-023-10937-9
pmid
37202742
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Yusheng Chen
[1]
Fengjin Ma
[2]
Zhe Zhang
[3]
Yang Guo
[4]
Hanwei Shen
[5]
Hang Chen
journal
BMC cancer
year
2023
abstract
BACKGROUND: PVT1, a previously uncharacterized lncRNA, was identified as a critical regulator involved in multiple functions in tumor, including cell proliferation, cell motility, angiogenesis and so on. However, the clinical significance and underlying mechanism of PVT1 was not be fully explored in glioma. METHODS: In this study, 1210 glioma samples with transcriptome data from three independent databases (CGGA RNA-seq, TCGA RNA-seq and GSE16011 cohorts) were enrolled in this study. Clinical information and genomic profiles containing somatic mutations and DNA copy numbers were collected from TCGA cohort. The R software was performed for statistical calculations and graphics. Furthermore, we validated the function of PVT1 in vitro. RESULTS: The results indicated that higher PVT1 expression was associated with aggressive progression of glioma. Cases with higher PVT1 expression always accompanied by PTEN and EGFR alteration. In addition, functional analyses and western blot results suggested that PVT1 inhibited the sensitivity of TMZ chemotherapy via JAK/STAT signaling. Meanwhile, knockdown of PVT1 increased the sensitivity of TZM chemotherapy in vitro. Finally, high PVT1 expression was associated with reduced survival time and may serve as a strong prognostic indicator for gliomas. CONCLUSIONS: This study demonstrated that PVT1 expression strongly correlated with tumor progression and chemo-resistance. PVT1 may become a potential biomarker for the diagnosis and treatment in glioma.
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The Kaplan-Meier analysis was performed to evaluated the overall survival of glioma patients using the “survival” and “survminer” packages.
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The Kaplan-Meier analysis was performed to evaluated the overall survival of glioma patients using the “survival” and “survminer” packages.
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Data AvailabilityThe datasets collected were the Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn), The Cancer Genome Atlas (TCGA) database (http://cancergenome.nih.gov/)[32].
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Data AvailabilityThe datasets collected were the Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn), The Cancer Genome Atlas (TCGA) database (http://cancergenome.nih.gov/)[32].
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In CGGA cohort, the Kaplan-Meier analysis verified that gliomas with higher expression levels of PVT1 experienced significantly shorter overall survival (OS) in both whole gliomas (p < 0.0001) and GBM (p = 0.0064) (Fig. 3A, B).
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sections[15] "PVT1 predicted worse survival in gliomas" paragraph 2
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In CGGA cohort, the Kaplan-Meier analysis verified that gliomas with higher expression levels of PVT1 experienced significantly shorter overall survival (OS) in both whole gliomas (p < 0.0001) and GBM (p = 0.0064) (Fig. 3A, B).
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In CGGA cohort, the Kaplan-Meier analysis verified that gliomas with higher expression levels of PVT1 experienced significantly shorter overall survival (OS) in both whole gliomas (p < 0.0001) and GBM (p = 0.0064) (Fig. 3A, B).
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Data AvailabilityThe datasets collected were the Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn), The Cancer Genome Atlas (TCGA) database (http://cancergenome.nih.gov/)[32].
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ration. In addition, functional analyses and western blot results suggested that PVT1 inhibited the se
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motherapy via JAK/STAT signaling. Meanwhile, knockdown of PVT1 increased the sensitivity of TZM che
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cal748357 Mesenchymal689284 Cell culture and transfection Human glioma cell lines U87 and LN229 were p
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Complete file
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However, the clinical significance and underlying mechanism of PVT1 was not be fully explored in glioma.\nMETHODS: In this study, 1210 glioma samples with transcriptome data from three independent databases (CGGA RNA-seq, TCGA RNA-seq and GSE16011 cohorts) were enrolled in this study. Clinical information and genomic profiles containing somatic mutations and DNA copy numbers were collected from TCGA cohort. The R software was performed for statistical calculations and graphics. Furthermore, we validated the function of PVT1 in vitro.\nRESULTS: The results indicated that higher PVT1 expression was associated with aggressive progression of glioma. Cases with higher PVT1 expression always accompanied by PTEN and EGFR alteration. In addition, functional analyses and western blot results suggested that PVT1 inhibited the sensitivity of TMZ chemotherapy via JAK/STAT signaling. Meanwhile, knockdown of PVT1 increased the sensitivity of TZM chemotherapy in vitro. 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