Evidence map›Paper›PMID 29531214›Full record

ArticleCell death & disease2018

LASP1 promotes nasopharyngeal carcinoma progression through negatively regulation of the tumor suppressor PTEN.

Qingzu Gao, Lihua Tang, Ling Wu, Kaitao Li, Hui Wang, Weidong Li, Juan Wu, Mingyi Li, Shuang Wang, Liang Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. E3 ubiquitin ligases in nasopharyngeal carcinoma and implications for therapies.Journal of molecular medicine (Berlin, Germany) · 2023
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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 at 5 institutions in 1 country.

Qingzu GaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Lihua TangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ling WuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kaitao LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hui WangDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Weidong LiDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Juan WuDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Mingyi LiRadiotherapy Department, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Shuang WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China. shuangw@126.com.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China. liangsmu@foxmail.com.
Southern Medical University · CNGuangzhou Medical University Cancer Hospital · CNGuangzhou Medical University · CNNanfang Hospital · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LIM and SH3 protein 1 (LASP1) enhances tumor growth and metastasis in various cancers, but its role in nasopharyngeal carcinoma (NPC) remains unclear. Herein, we investigated the role of LASP1 in NPC and explored the underlying mechanisms in NPC. Clinically, overexpression of LASP1 is associated with tumor metastasis and poor prognosis of NPC patients. Gain-of-function and loss-of-function assays showed that LASP1 promoted NPC cell proliferation, metastasis, and invasion in vitro and in vivo. Mechanistically, we observed clear co-localization between LASP1 and PTEN in NPC cells. LASP1 interacted with PTEN and decreased the expression of PTEN in NPC. The ubiquitination assay indicated that LASP1 overexpression increased PTEN ubiquitination. PTEN was known as a tumor suppressor by negatively regulating phosphoinositide 3-kinase/AKT signaling pathway. Rescue experiments showed that PTEN weakened LASP1-mediated cell proliferation, migration, and invasive abilities and decreased the phosphorylation of AKT in NPC cells. Our findings suggest that LASP1 has a crucial role in NPC progression via LASP1/PTEN/AKT axis, highlighting LASP1 as a therapeutic target for NPC.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell ProliferationCohort StudiesCytoskeletal ProteinsDisease ProgressionHumansLIM Domain ProteinsMiceMice, NudeNasopharyngeal CarcinomaNasopharyngeal NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionAdaptor Proteins, Signal TransducingCytoskeletal ProteinsLASP1 protein, humanLIM Domain ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID29531214
PMCPMC5847534
OpenAlexW2790559294

What OpenQuestion holds

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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.