Evidence map›Paper›PMID 39209829›Full record

ArticleCell death discovery2024

CTDSPL2 promotes the progression of non-small lung cancer through PI3K/AKT signaling via JAK1.

Muzi Li, La Chen, Fangfang Yu, Huijuan Mei, Xingxing Ma, Keshuo Ding, Yanan Yang, Ziye Rong

Abstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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.

Muzi Li *Department of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
La Chen *Department of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Fangfang YuDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Huijuan MeiDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Xingxing MaDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Keshuo DingDepartment of Pathology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Yanan YangDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China. yang.yanan@ahmu.edu.cn.ORCID http://orcid.org/0009-0000-2717-7453
Ziye RongDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China. 2021500003@ahmu.edu.cn.ORCID http://orcid.org/0000-0001-5500-5894

Funding

University Natural Science Research Project of Anhui Province (Anhui Provincial Universities Natural Science Research Project) 2023AH050679
6 · The paper itself

Abstract

Carboxy-terminal domain small phosphatase like 2 (CTDSPL2), one of the haloacid dehalogenase phosphatases, is associated with several diseases including cancer. However, the role of CTDSPL2 and its regulatory mechanism in lung cancer remain unclear. Here, we aimed to explore the clinical implications, biological functions, and molecular mechanisms of CTDSPL2 in non-small cell lung cancer (NSCLC). CTDSPL2 was identified as a novel target of the tumor suppressor miR-193a-3p. CTDSPL2 expression was significantly elevated in NSCLC tissues. Database analysis showed that CTDSPL2 expression was negatively correlated with patient survival. Depletion of CTDSPL2 inhibited the proliferation, migration, and invasion of NSCLC cells, as well as tumor growth and metastasis in mouse models. Additionally, silencing of CTDSPL2 enhanced CD4

Identifiers

PMID39209829
PMCPMC11362329

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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.