Evidence map›Paper›PMID 38706904›Full record

ArticleJournal of Cancer2024

TRPV3 regulates Breast Cancer Cell Proliferation and Apoptosis by EGFR/AKT pathway.

Yan Xie, Hyo In Kim, Qianzhi Yang, Jinghao Wang, Wei Huang

Abstract read
In one paragraph

Article in Journal of Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. [Mechanism underlying carvacrol-induced alveolar bone repair via the phosphatidylinositol 3-kinase pathway in periodontal disease].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
    Article
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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.

Yan XieBasic Medicine College of Daqing Campus, Harbin Medical University-Daqing, Daqing, 163319, China.
Hyo In KimDepartment of Surgery, Beth Israel Deaconess Medical Center, Boston, MA, 02215, United States of America.
Qianzhi YangDepartment of Pharmacy, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Jinghao WangDepartment of Pharmacy, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Wei HuangDepartment of Pharmacology, Hainan Medical University, Haikou, 571199, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is one of the most common cancer types worldwide and the first cause of cancer-related deaths in women. Transient receptor potential vanillin 3 (TRPV3) has been preliminarily discovered to play an important role in various cancers, including BC. Here, we explored the effect of TRPV3 on breast cancer cells and its potential mechanism. TRPV3 level was measured in BC tissue and adjacent noncancerous breast tissue using real-time RT-PCR and Western blot. Wound healing was used to detect cell migration. MTT and EDU were detected cell proliferation. TUNEL and Caspase-3 activity were used to detect cell apoptosis. We found that TRPV3 expression significantly increased in both human BC tissues and breast cells line. TRPV3 siRNA (TRPV3 inhibition) dramatically suppressed cell migration and proliferation, promoted the apoptosis, and decreased [Ca

Indexed as

apoptosisbreast cancerEGFRproliferationTRPV3

Identifiers

PMID38706904
PMCPMC11064276

What OpenQuestion holds

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LicenceCC BY
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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.