Evidence map›Paper›PMID 35130633›Full record

ArticleActa biochimica et biophysica Sinica2022

Upregulation of CENPM facilitates lung adenocarcinoma progression via PI3K/AKT/mTOR signaling pathway.

Chao Liu, Yun Wang, Yuyang Dao, Shuting Wang, Fei Hou, Zhixian Yang, Pengjie Liu, Juan Lv, Ling Lv, Gaofeng Li and 2 more

Open access · greenAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

12 authors at 1 institution in 1 country.

Chao LiuDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Yun WangDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Yuyang DaoDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Shuting WangDepartment of Thoracic Surgery, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Fei HouDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Zhixian YangDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Pengjie LiuDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Juan LvDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Ling LvDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Gaofeng LiDepartment of Thoracic Surgery, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Youjun ZhouDepartment of Nuclear Medicine, the Affiliated Yan'an Hospital of Kunming Medical College, Kunming 650118, China.
Zhiyong DengDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, the Third Affiliated Hospital of Kunming Medical College, Kunming 650118, China.
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Centromere protein M (CENPM) is essential for chromosome separation during mitosis. However, its roles in lung adenocarcinoma (LUAD) progression and metastasis remain unknown. In this study, we aimed to explore the effects of CENPM on LUAD progression as well as the underlying mechanisms. We analyzed the expression of CENPM and its correlation with clinicopathological characteristics using GEO LUAD chip datasets and TCGA dataset. We further investigated the impact of CENPM on LUAD and . In silico analysis and qRT-PCR revealed that CENPM is upregulated in LUAD compared with that in normal lung tissues. Via gain/loss-of-function assays, we further found that CENPM promotes the LUAD cell cycle, cell proliferation, migration and invasion, and inhibits cell apoptosis. The study showed that loss of CENPM inhibits the growth of A549 xenografts. Furthermore, we found that CENPM can promote the phosphorylation of mTOR rather than directly affect the mTOR content. Inhibition of mTOR activity abrogates the promoting effects of CENPM on cell cycle progression, cell proliferation, migration and invasion. Taken together, these results show that CENPM plays an important role in the growth and metastasis of LUAD and may be a promising therapeutic target in LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCell Cycle ProteinsCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesUp-RegulationCell Cycle ProteinsCENPM protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCENPMlung adenocarcinomaPI3K/AKT/mTOR signaling pathway

Identifiers

PMID35130633
PMCPMC9909302
OpenAlexW4205468790

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.