LncRNA SAMMSON Knockdown Inhibits the Malignancy of Glioblastoma Cells by Inactivation of the PI3K/Akt Pathway

Ni, Hongzao; Wang, Kai; Xie, Peng; Zuo, Jiandong; Liu, Wenguang; Liu, Chun

doi:10.1007/s10571-020-00833-2

Cited by 20 publications

(13 citation statements)

References 34 publications

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“…The lncRNA, SAMMSON, is overexpressed in GBM tumors and cell lines. SAMMSON silencing brought about inhibition of GBM cell viability and invasive properties by partially regulating the PI3K/Akt signaling pathway (H. Ni et al, 2021).…”

Section: Pathways Affected By Lncrnas In the Course Of Gbm Metastasismentioning

confidence: 99%

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Metastasis associated long noncoding RNAs in glioblastoma: Biomarkers and therapeutic targets

Yadav

Kulshreshtha

2021

Journal Cellular Physiology

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Glioblastoma (GBM) is the most aggressive, malignant, and therapeutically challenging Grade IV tumor of the brain. Although the possibility of distant metastasis is extremely rare, GBM is known to cause intracranial metastasis forming aggressive secondary lesions resulting in a dismal prognosis. Metastasis also plays an important role in tumor dissemination and recurrence making GBM largely incurable. Recent studies have indicated the importance of long noncoding RNAs (lncRNAs) in GBM metastasis. lncRNAs are a class of regulatory noncoding RNAs (>200 nt) that interact with DNA, RNA, and proteins to regulate various biological processes. This is the first comprehensive review summarizing the lncRNAs associated with GBM metastasis and the underlying molecular mechanism involved in migration/invasion. We also highlight the complex network of lncRNA/miRNA/protein that collaborate/compete to regulate metastasis-associated genes. Many of these lncRNAs also show attractive potential as diagnostic/prognostic biomarkers. Finally, we discuss various therapeutic strategies and potential applications of lncRNAs as therapeutic targets for the treatment of GBM.

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Section: Pathways Affected By Lncrnas In the Course Of Gbm Metastasismentioning

confidence: 99%

“…EMT, epithelial to mesenchymal transition; lncRNA, long non-coding RNA Wnt/β, and NF-kB pathway in glioma (Q.. The lncRNA, SAMMSON, is overexpressed in GBM tumors and cell lines.SAMMSON silencing brought about inhibition of GBM cell viability and invasive properties by partially regulating the PI3K/Akt signaling pathway (H Ni et al, 2021)…”

mentioning

confidence: 99%

Metastasis associated long noncoding RNAs in glioblastoma: Biomarkers and therapeutic targets

Yadav

Kulshreshtha

2021

Journal Cellular Physiology

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“…[13][14][15] In recent years, authoritative research has uncovered the aberrant expression of lncRNAs in GBM and validated lncRNAs as promoters or inhibitors of cancer-associated processes. [16][17][18] Similar to lncRNAs, microRNAs (miRNAs) comprise another class of single-stranded, non-coding RNA transcripts, with a length ranging from 17 to 24 nucleotides. 19 miRNAs may directly interact with the 3ʹuntranslated region (3ʹ-UTR) of target genes and inhibit their expression, consequently causing mRNA degradation or translation inhibition.…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression

Cheng

Liu

Zhang

et al. 2021

CMAR

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Background: The dysregulation of long non-coding RNAs is a frequent finding in glioblastoma (GBM) and is considered as a crucial mechanism contributing to GBM oncogenesis and progression. The biological roles and underlying mechanisms of action of UBA6 antisense RNA 1 (UBA6-AS1) in GBM have been rarely investigated. Therefore, the aim of the present study was to investigate in detail the role of UBA6-AS1 in the modulation of the malignant properties of GBM and explore the possible underlying mechanism(s). Methods: The expression of UBA6-AS1 in GBM was determined via reverse transcriptionquantitative PCR. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and in vivo tumorigenicity assay were applied to elucidate the biological effects of UBA6-AS1 on GBM cells. The possible biological events associated with UBA6-AS1 were investigated by luciferase reporter, RNA immunoprecipitation (RIP) and rescue assays. Results: UBA6-AS1 was overexpressed in GBM, which was consistent with the data from The Cancer Genome Atlas database. In the case of UBA6-AS1 depletion, GBM cell proliferation, migration and invasion were notably decreased and cell apoptosis was enhanced in vitro. Additionally, knockdown of UBA6-AS1 suppressed the proliferation of GBM cells in vivo. Mechanistically, UBA6-AS1 functioned as a competing endogenous RNA by adsorbing miR-760 and, consequently, upregulating homeobox A2 (HOXA2) expression. Rescue experiments demonstrated that the UBA6-AS1 silencing-mediated regulatory effects on GBM cells were reversed by the decrease of miR-760 or restoration of HOXA2 expression. Conclusion: Therefore, the results of the present study revealed that UBA6-AS1 promoted the malignant progression of GBM via targeting the miR-760/HOXA2 axis, thereby representing a promising effective target for the treatment of GBM.

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“… 14 It is still unknown whether miR-130a participates in IA. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON, a well-studied cancer-related lncRNA, 15 across IA samples. SAMMSON plays a critical role in cancer biology by interacting with critical signal pathways involved in cancer development, such as PI3K/Akt Pathway.…”

Section: Introductionmentioning

confidence: 79%

“…SAMMSON plays a critical role in cancer biology by interacting with critical signal pathways involved in cancer development, such as PI3K/Akt Pathway. 15 However, the involvement of SAMMSON in IA is unknown. This study analyzed the potential interaction between SAMMSON and miR-130a in IA.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

Pan

Gao

Wan

et al. 2021

NDT

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Background MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Therefore, we further studied the crosstalk between SAMMSON and miR-130a in IA. Methods SAMMSON and miR-130a expression were measured using RT-qPCR. SAMMSON subcellular location was analyzed with nuclear fractionation assay. Their direct interaction was explored with RNA pull-down assay. The role of SAMMSON in miR-130a maturation was studied with overexpression analysis. VSMC cell proliferation was analyzed with BrdU assay. Results SAMMSON and premature miR-130a were deregulated in IA, while mature miR-130a was upregulated in IA. SAMMSON is localized in both the nucleus and cytoplasm, and direct interaction between SAMMSON and miR-130a was observed. SAMMSON overexpression suppressed miR-130a maturation in VSMCs and reduced the enhancing effects of miR-130a on VSMC cell proliferation. Conclusion SAMMSON is overexpressed in IA and suppresses VSMC proliferation via inhibiting miR-130a maturation.

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LncRNA SAMMSON Knockdown Inhibits the Malignancy of Glioblastoma Cells by Inactivation of the PI3K/Akt Pathway

Cited by 20 publications

References 34 publications

Metastasis associated long noncoding RNAs in glioblastoma: Biomarkers and therapeutic targets

Metastasis associated long noncoding RNAs in glioblastoma: Biomarkers and therapeutic targets

Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

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