Evidence map›Paper›PMID 33469269›Full record

ArticleDrug design, development and therapy2021

Combination of Sodium Cantharidinate with Cisplatin Synergistically Hampers Growth of Cervical Cancer.

Xiangxun Chen, Mengxi Zhou, Wenjie Fan, Mingwei Yang, Lin Yang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 45% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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.

Xiangxun ChenDepartment of Radiation Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, People's Republic of China.
Mengxi ZhouDepartment of Radiation Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, People's Republic of China.
Wenjie FanDepartment of Radiation Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, People's Republic of China.
Mingwei YangDepartment of Radiation Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, People's Republic of China.
Lin YangDepartment of Radiation Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, People's Republic of China.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium cantharidinate (SC) has been broadly applied in lung cancer treatment in China, while its specific function in cervical cancer (CC), a great contributor to death of female reproductive system cancers, remains unclear. Our research evaluated the anti-tumor effects of SC in CC and the mechanism involved.

methodsFirst, cisplatin (DDP)-resistant Caski-1 and ME180 cell lines were developed and treated with SC. The effects of SC on CC cell growth were then evaluated. Subsequently, the genes targeted by SC were predicted via the bioinformatics website. The correlations between PTPN1 expression and tumor stage, lymph node metastasis and tumor differentiation were examined. We further conducted rescue experiments by overexpressing PTPN1 in CC cells, followed by SC and cisplatin treatments. The activation of the PI3K/AKT pathway in CC cells, and the effect of SC on the growth and drug resistance of Caski-1 cells in vivo were investigated.

resultsThe sensitivity of Caski-1 and ME180 cells to DDP was increased after SC treatment, which also enhanced the inhibitory effect of DDP on the cell growth. By prediction, we found that SC could target PTPN1. Patients with high expression of PTPN1 had higher clinical stage, lymph node metastasis and lower tumor differentiation. SC inhibited PTPN1 expression. Overexpression of PTPN1 attenuated the effect of SC. Furthermore, PTPN1 activated the PI3K/AKT pathway. Moreover, SC treatment inhibited the growth and drug resistance of Caski-1 cells in vivo.

conclusionSC promotes drug sensitivity of CC cells to DDP by targeting PTPN1, thereby impairing the PI3K/AKT pathway.

Indexed as

Antineoplastic AgentsCantharidinCell Line, TumorCell ProliferationCisplatinDrug CombinationsDrug Screening Assays, AntitumorFemaleHumansMolecular ConformationProtein Tyrosine Phosphatase, Non-Receptor Type 1Uterine Cervical NeoplasmsAntineoplastic AgentsCantharidinCisplatinDrug CombinationsProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humancervical cancercisplatinPTPN1sodium cantharidinatethe PI3K/AKT pathway

Identifiers

PMID33469269
PMCPMC7812528
OpenAlexW3118955068

What OpenQuestion holds

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LicenceCC BY-NC
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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.