Evidence map›Paper›PMID 29980193›Full record

ArticleBMC cancer2018

LIM and SH3 protein 1 regulates cell growth and chemosensitivity of human glioblastoma via the PI3K/AKT pathway.

Chuanhong Zhong, Yitian Chen, Bei Tao, Lilei Peng, Tangming Peng, Xiaobo Yang, Xiangguo Xia, Ligang Chen

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. AGenome research · 2020
    Article
  18. Article
  19. Article
  20. Article
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

8 authors at 2 institutions in 1 country.

Chuanhong ZhongNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Yitian ChenDepartment of Clinical Medicine, Medical College of Soochow University, Suzhou, China.
Bei TaoRheumatism Department, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Lilei PengNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Tangming PengNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Xiaobo YangNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Xiangguo XiaNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Ligang ChenNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. chenligang199066@163.com.
Affiliated Hospital of Southwest Medical University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLIM and SH3 protein 1 (LASP1) is upregulated in several types of human cancer and implicated in cancer progression. However, the expression and intrinsic function of LASP1 in glioblastoma (GBM) remains unclear.

methodOncomine and The Cancer Genome Atlas (TCGA) database was analyzed for the expression and clinical significance of LASP1 in GBM. LASP1 mRNA and protein level were measured by qRT-PCR and western blotting. The effect of LASP1 on GBM proliferation was examined by MTT assay and colony formation assay, the effect of LASP1 on sensitivity of Temozolomide was measured by flow cytometry and subcutaneous tumor model. The association between LASP1 and PI3K/AKT signaling was assessed by western blotting.

resultsOncomine GBM dataset analysis indicated LASP1 is significantly upregulated in GBM tissues compared to normal tissues. GBM dataset from The Cancer Genome Atlas (TCGA) revealed that high LASP1 expression is related to poor overall survival. LASP1 mRNA and protein in clinical specimens and tumor cell lines are frequently overexpressed. LASP1 knockdown dramatically suppressed U87 and U251 cell proliferation. Silencing LASP1 potentiated cell chemosensitivity to temozolomide in vitro, LASP1 knockdown inhibited tumor growth and enhanced the therapeutic effect of temozolomide in vivo. TCGA dataset analysis indicated LASP1 was correlated with PI3K/AKT signaling pathway, and LASP1 deletion inhibited this pathway. Combination treatment with PI3K/AKT pathway inhibitor LY294002 dramatically accelerated the suppression effect of temozolomide.

conclusionLASP1 may function as an oncogene in GBM and regulate cell proliferation and chemosensitivity in a PI3K/AKT-dependent mechanism. Thus, the LASP1/PI3K/AKT axis is a promising target and therapeutic strategy for GBM treatment.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Line, TumorCell ProliferationCytoskeletal ProteinsDrug Resistance, NeoplasmGlioblastomaHumansLIM Domain ProteinsMaleMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTemozolomideAdaptor Proteins, Signal TransducingCytoskeletal ProteinsLASP1 protein, humanLIM Domain ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTemozolomideGlioblastomaLIM and SH3 protein 1PI3K/AKT pathwayTemozolomide

Identifiers

PMID29980193
PMCPMC6035445
OpenAlexW2826737886

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.