Evidence map›Paper›PMID 39165489›Full record

ArticleInternational journal of genomics2024

SKF96365 Inhibits Tumor Proliferation by Inducing Apoptosis and Autophagy in Human Esophageal Squamous Cell Carcinoma.

Jiaxin Zhang, Huiqiong Han, Yihan Liu, Jiayao Xu, Daidi Zhang, Wenjia Wang, Yaping Gao, Zhengrui Li, Yanru Qin

Abstract read
In one paragraph

Article in International journal of genomics, 2024. 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
–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

1 citing paper in PubMed.

  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

9 authors.

Jiaxin ZhangDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.ORCID https://orcid.org/0009-0009-2216-0543
Huiqiong HanDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Yihan LiuDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Jiayao XuDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Daidi ZhangDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Wenjia WangDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Yaping GaoDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Zhengrui LiDepartment of Oral and Maxillofacial-Head and Neck Oncology Shanghai Ninth People's Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.ORCID https://orcid.org/0000-0003-4923-0088
Yanru QinDepartment of Oncology The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.ORCID https://orcid.org/0000-0003-2175-9617

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium channel blockers are emerging as a new generation of attractive anticancer drugs. SKF96365, originally thought to be a store-operated calcium entry (SOCE) inhibitor, is now often used as a TRPC channel blocker and is widely used in medical diagnostics. SKF96365 has shown antitumor effects on a variety of cancer cell lines. The objective of this study was to investigate the anticancer effect of SKF96365 on esophageal cancer in vivo and in vitro. Cell Counting Kit-8 (CCK-8) and colony formation were used to test the proliferation inhibition of SKF96365 on cell lines. Western blot and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to detect cell apoptosis rates. In addition, we demonstrated the antitumor effect of SKF96365 in vivo in xenografted mice. As a result, SKF96365 significantly inhibited the proliferation of K510, K30, and EC9706 in vitro. SKF96365 induces apoptosis in three cell lines through the poly(adenosine diphosphate-ribose) polymerase (PARP), caspase-9, and BCL-2 pathways in a dose-dependent and time-dependent manner. Moreover, SKF96365 treatment also induced apoptosis and inhibited tumor growth in nude mice. The calcium channel TRPC1 was significantly downregulated by SKF96365. Autophagy was also induced during the treatment of SKF96365. In summary, SKF96365 induces apoptosis (PARP, caspase-9, and BCL-2) and autophagy (LC3-A/B) by inhibiting TRPC1 in esophageal cancer cells, thereby inhibiting tumor growth.

Indexed as

apoptosisautophagycalcium channelesophageal squamous cell carcinomaSKF96365TRPC1

Identifiers

PMID39165489
PMCPMC11335422

What Socratic holds

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LicenceCC BY
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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 Socratic graph.