Evidence map›Paper›PMID 35939116›Full record

ArticleJournal of cancer research and clinical oncology2023

Effects and mechanisms of GSG2 in esophageal cancer progression.

Chong Geng, Qiang Wang, Peng-Fei Xing, Min Wang, Shao-Dong Tong, Ju-Ying Zhou

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 57% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 2 institutions in 1 country.

Chong Geng *Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Jiangsu Province, No.188 Shizi street, Suzhou, 215006, China.
Qiang Wang *Department of Radiation Oncology, Xuzhou Cancer Hospital, Xuzhou, 221005, China.
Peng-Fei XingDepartment of Radiotherapy Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Min WangDepartment of Radiation Oncology, Xuzhou Cancer Hospital, Xuzhou, 221005, China.
Shao-Dong TongDepartment of Radiation Oncology, Xuzhou Cancer Hospital, Xuzhou, 221005, China.
Ju-Ying ZhouDepartment of Radiation Oncology, The First Affiliated Hospital of Soochow University, Jiangsu Province, No.188 Shizi street, Suzhou, 215006, China. zhoujuyingsy@163.com.
Jiangsu University · CNSoochow University · CN

Funding

Xuzhou Science and Technology Plan Project KC19186
6 · The paper itself

Abstract

backgroundEsophageal cancer was recognized as one of the malignant tumors with poor prognosis. Germ cell associated 2 (GSG2) has been reported to be of great significance in cell growth and tumor formation. This study aimed to investigate the biological function and molecular mechanism of GSG2 in esophageal cancer.

methodsFirst, relationship between GSG2 expression and tumor characteristics in esophageal cancer patients was analyzed through immunohistochemical (IHC) staining. MTT assay, flow cytometry, cloning formation assay, wound-healing assay and Transwell assay were used to determine proliferation, apoptosis and migration of esophageal cancer cell with GSG2 knockdown in vitro. Expression of apoptosis related proteins and downstream pathway proteins after GSG2 knockdown were detected through Human Apoptosis Antibody Array and western blot analysis. The GSG2 knockdown function in vivo was explored through a xenograft tumor model.

resultsGSG2 was highly expressed in tumor tissues, which has clinical significance in predicting the malignant degree of patients with esophageal cancer. In addition, GSG2 knockdown significantly inhibited a variety of malignant biological behaviors of esophageal cancer cells, such as inhibiting proliferation, reducing colony formation, promoting apoptosis, hindering migration. The decrease of GSG2 expression in esophageal cancer cells can inhibit the xenograft tumor growth.

conclusionsIn conclusion, GSG2 was involved in esophageal cancer progression and development, which may provide an effective molecular target for the treatment of esophageal cancer in the future.

Indexed as

Esophageal NeoplasmsApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesHASPIN protein, humanIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesEsophageal cancerGSG2MigrationProliferation

Identifiers

PMID35939116
PMCPMC11796740
OpenAlexW4290648656

What OpenQuestion holds

Textmetadata
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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.