Evidence map›Paper›PMID 35866593›Full record

ArticleOncology reports2022

Leptin stimulates migration and invasion and maintains cancer stem‑like properties in gastric cancer cells.

Ki Bum Park, Eun Young Kim, Hyungmin Chin, Dong Joon Yoon, Kyong-Hwa Jun

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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  20. Anti-Obesity Effect of Chitoglucan in High-Fat-Induced Obesity Mice.International journal of environmental research and public health · 2022
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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

5 authors at 2 institutions in 1 country.

Ki Bum ParkDepartment of Surgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Paldal‑gu, Suwon‑si, Gyeonggi‑do 16247, Republic of Korea.
Eun Young KimDepartment of Surgery, Uijeongbu St. Mary Hospital, College of Medicine, The Catholic University of Korea, Uijeongbu‑si, Gyeonggi‑do 11765, Republic of Korea.
Hyungmin ChinDepartment of Surgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Paldal‑gu, Suwon‑si, Gyeonggi‑do 16247, Republic of Korea.
Dong Joon YoonClinical Medical Laboratory, St. Vincent's Hospital, Paldal‑gu, Suwon‑si, Gyeonggi‑do 16247, Republic of Korea.
Kyong-Hwa JunDepartment of Surgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Paldal‑gu, Suwon‑si, Gyeonggi‑do 16247, Republic of Korea.
The Catholic University of Korea St. Vincent's Hospital · KRThe Catholic University of Korea Uijeongbu St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is a risk factor for various types of cancer. Leptin, an adipocyte‑derived hormone, may stimulate the proliferation of gastric cancer cells. However, the effect of leptin and underlying mechanism in gastric cancer remain unclear. In the present study, the role of leptin in gastric cancer was evaluated. The effect of leptin on the JAK‑STAT and MEK signaling pathways was investigated in gastric cancer cells using wound‑healing and cell invasion assays, immunoblotting and inhibition studies. Cancer‑initiating cells derived from gastric cancer cells were used to investigate the effect of leptin on the maintenance of stemness and epithelial‑mesenchymal transition (EMT) by immunoblotting. Clinicopathological characteristics including the serum leptin level and overall survival (OS) were analyzed in patients with (n=23) and without (n=23) obesity. Leptin induced the migration and invasion of gastric cancer cells by activating AKT and ERK and upregulating vascular endothelial growth factor (VEGF). Leptin increased the mRNA and protein levels of markers of stemness (CD44) and the EMT (Snail and N‑cadherin). Pharmacological inhibitors of the JAK‑STAT and MEK signaling pathways decreased leptin‑induced migration and invasion, and the expression of VEGF. Obesity was associated with an elevated leptin level and body mass index was positively correlated with the leptin level (P=0.001 for both). The 5‑year OS rate was not significantly different between the two groups (P=0.098). Leptin stimulates the migration and invasion of gastric cancer cells by activating the JAK‑STAT and MEK pathways, and contributes to the maintenance of cancer stemness and metastatic potential. The present findings support an adverse effect of obesity in gastric cancer. Consequently, targeting of leptin‑associated signaling pathways may have therapeutic potential for gastric cancer.

Indexed as

LeptinNeoplastic Stem CellsStomach NeoplasmsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansMitogen-Activated Protein Kinase KinasesObesityVascular Endothelial Growth Factor ALeptinMitogen-Activated Protein Kinase KinasesVascular Endothelial Growth Factor Acancer stemnesscell invasioncell migrationgastric cancerleptin

Identifiers

PMID35866593
PMCPMC9350977
OpenAlexW4286498636

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.