Evidence map›Paper›PMID 37373457›Full record

ArticleInternational journal of molecular sciences2023

CD109 Promotes Drug Resistance in A2780 Ovarian Cancer Cells by Regulating the STAT3-NOTCH1 Signaling Axis.

Jun Se Kim, Min Joo Shin, Seo Yul Lee, Dae Kyoung Kim, Kyung-Un Choi, Dong-Soo Suh, Dayea Kim, Jae Ho Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 14 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

8 authors at 2 institutions in 1 country.

Jun Se KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.ORCID 0000-0003-4321-8854
Min Joo ShinDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
Seo Yul LeeDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.ORCID 0000-0003-4415-0070
Dae Kyoung KimHicelltech Inc., Yangsan 50612, Republic of Korea.
Kyung-Un ChoiDepartment of Pathology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
Dong-Soo SuhDepartment of Obstetrics and Gynecology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.ORCID 0000-0001-5785-4355
Dayea KimNew Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation (K-MEDI hub), Daegu 41061, Republic of Korea.
Jae Ho KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.ORCID 0000-0003-4323-4790
Pusan National University · KRDaegu-Gyeongbuk Medical Innovation Foundation · KR

Funding

National Research Foundation of Korea NRF-2020R1A2C2011880National Research Foundation of Korea NRF-2020R1I1A3073064National Research Foundation of Korea NRF-2022R1A5A2027161
6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy owing to relapse caused by resistance to chemotherapy. We previously reported that cluster of differentiation 109 (CD109) expression is positively correlated with poor prognosis and chemoresistance in patients with EOC. To further explore the role of CD109 in EOC, we explored the signaling mechanism of CD109-induced drug resistance. We found that CD109 expression was upregulated in doxorubicin-resistant EOC cells (A2780-R) compared with that in their parental cells. In EOC cells (A2780 and A2780-R), the expression level of CD109 was positively correlated with the expression level of ATP-binding cassette (ABC) transporters, such as ABCB1 and ABCG2, and paclitaxel (PTX) resistance. Using a xenograft mouse model, it was confirmed that PTX administration in xenografts of CD109-silenced A2780-R cells significantly attenuated in vivo tumor growth. The treatment of CD109-overexpressed A2780 cells with cryptotanshinone (CPT), a signal transducer and activator of transcription 3 (STAT3) inhibitor, inhibited the CD109 overexpression-induced activation of STAT3 and neurogenic locus notch homolog protein 1 (NOTCH1), suggesting a STAT3-NOTCH1 signaling axis. The combined treatment of CD109-overexpressed A2780 cells with CPT and N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT), a NOTCH inhibitor, markedly abrogated PTX resistance. These results suggest that CD109 plays a key role in the acquisition of drug resistance by activating the STAT3-NOTCH1 signaling axis in patients with EOC.

Indexed as

Ovarian NeoplasmsAnimalsAntigens, CDATP-Binding Cassette TransportersCarcinoma, Ovarian EpithelialCell Line, TumorDrug Resistance, NeoplasmFemaleGPI-Linked ProteinsHumansMiceNeoplasm ProteinsNeoplasm Recurrence, LocalPaclitaxelReceptor, Notch1STAT3 Transcription FactorAntigens, CDATP-Binding Cassette TransportersCD109 protein, humanGPI-Linked ProteinsNeoplasm ProteinsNOTCH1 protein, humanPaclitaxelReceptor, Notch1STAT3 protein, humanSTAT3 Transcription FactorA2780cluster of differentiation 109 (CD109)drug resistanceepithelial ovarian cancerneurogenic locus notch homolog protein 1 (NOTCH1)signal transducer and activator of transcription 3 (STAT3)

Identifiers

PMID37373457
PMCPMC10299649
OpenAlexW4381149394

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.