Evidence map›Paper›PMID 36815969›Full record

ArticleExperimental and therapeutic medicine2023

Knockdown of NCAPG promotes the apoptosis and inhibits the invasion and migration of triple‑negative breast cancer MDA‑MB‑231 cells via regulation of EGFR/JAK/STAT3 signaling.

Juanyun Li, Jialu Zheng, Baohang Lin, Hao Sun, Shan Lu, Dandan Wang, Hongjun Huo

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2023. 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
1.0field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. In smokers, the axis NCAPG/hsa-let-7b-5p/TMPO-AS1 promotes lung adenocarcinoma.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
    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

7 authors at 1 institution in 1 country.

Juanyun LiDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Jialu ZhengDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Baohang LinDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Hao SunDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Shan LuDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Dandan WangDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Hongjun HuoDepartment of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China.
Longgang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer and the treatment options are extremely limited. Non-SMC condensing I complex subunit G (NCAPG) expression is upregulated in TNBC, but its specific regulatory mechanism in TNBC has not been previously reported. The expression levels of NCAPG in TNBC were analyzed using data obtained from the UALCAN database. RT-qPCR and western blotting were used to detect the expression of NCAPG in various breast cancer cell lines. The expression of NCAPG was knocked down, and cell viability was then detected using a CCK-8 assay, apoptosis was detected using a TUNEL assay, and the expression of the apoptosis-related proteins Bcl-2, Bax and Bad were detected by western blotting. Wound healing and Transwell assays were used to assess migration and invasion. Western blotting was also used to determine the expression levels of migration and invasion-related proteins MMP2 and MMP9, as well as EGFR/JAK/STAT3 pathway-related proteins. Following exogenous treatment with EGF and the JAK/STAT3 signaling pathway agonist colivelin, cell viability, apoptosis, invasion and migration were assessed. The expression of NCAPG in TNBC MDA-MB-231 cells was significantly increased. Inhibition of NCAPG inhibited the activity, promoted apoptosis, and inhibited the invasion and migration of TNBC MDA-MB-231 cells, potentially via regulation of the EGFR/JAK/STAT3 signaling pathway. In conclusion, downregulation of NCAPG can promote apoptosis and inhibit invasion and migration of TNBC MDA-MB-231 cells via EGFR/JAK/STAT3 signaling.

Indexed as

apoptosisEGFR/JAK/STAT3invasionmigrationNCAPGtriple-negative breast cancer

Identifiers

PMID36815969
PMCPMC9932631
OpenAlexW4318776940

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.