Evidence map›Paper›PMID 36038736›Full record

ArticleApoptosis : an international journal on programmed cell death2022

CACNA1C-AS2 inhibits cell proliferation and suppresses cell migration and invasion via targeting FBXO45 and PI3K/AKT/mTOR pathways in glioma.

Tong Cao, Yue Cui, Yingying Wang, Linhui Wu, Ke Yu, Kai Chen, Jun Xia, Yuyun Li, Zhiwei Peter Wang, Jia Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Tong Cao *Department of Clinical Laboratory, the First Affiliated Hospital of Bengbu Medical College, Bengbu, 233004, Anhui, China.
Yue Cui *Bengbu Medical College Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Yingying Wang *Bengbu Medical College Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Linhui WuBengbu Medical College Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Ke YuBengbu Medical College Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Kai ChenBengbu Medical College Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Jun XiaDepartment of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai Street, Bengbu, 233030, Anhui, China.
Yuyun LiDepartment of Clinical Laboratory Diagnostics, School of Laboratory Medicine, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Zhiwei Peter WangDepartment of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai Street, Bengbu, 233030, Anhui, China. zhiweichina@126.com.ORCID 0000-0002-6465-7779
Jia MaDepartment of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai Street, Bengbu, 233030, Anhui, China. majiamj10@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most common brain cancer with a poor prognosis, and its underlying molecular mechanisms still needs to be further explored. In the current study, we discovered that an antisense lncRNA, CACNA1C-AS2, suppressed growth, migration and invasion of glioma cells, suggesting that CACNA1C-AS2 functions as a tumor suppressor. Furthermore, we found that CACNA1C-AS2 negatively regulated Fbxo45 protein expression in glioma cells. Impressively, extensive experimental results revealed that Fbxo45 accelerated growth, migration and invasion of glioma cells. Clinically, increased Fbxo45 expression was observed in 75 human glioma tissue samples. Moreover, in vivo experiments also demonstrated that Fbxo45 overexpression enhanced tumor growth in mice. Especially, we further identified that Fbxo45 activated mTORC1 rather than mTORC2 through PI3K/AKT signaling to promote cell growth and motility in glioma cells. Rescue experiments also exhibited that CACNA1C-AS2 inhibited cell growth and motility partly through down-regulating Fbxo45 expression in glioma. Our results provide the novel insights into the critical role of CACNA1C-AS2/Fbxo45/mTOR axis involved in regulating glioma tumorigenesis and progression, and further indicate that CACNA1C-AS2 and Fbxo45 may be the potential biomarkers and therapeutic targets for glioma.

Indexed as

F-Box ProteinsGliomaMicroRNAsAnimalsApoptosisCalcium Channels, L-TypeCell Line, TumorCell MovementCell ProliferationHumansMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCACNA1C protein, humanCACNA1C protein, mouseCalcium Channels, L-TypeF-Box ProteinsFBXO45 protein, humanFbxo45 protein, mouseMicroRNAsMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCACNA1C-AS2Fbxo45GliomaGrowthmTOR

Identifiers

PMID36038736

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.