Evidence map›Paper›PMID 35592390›Full record

ArticleMolecular therapy oncolytics2022

Inhibition of MEK-ERK pathway enhances oncolytic vaccinia virus replication in doxorubicin-resistant ovarian cancer.

Seoyul Lee, Wookyeom Yang, Dae Kyoung Kim, Hojun Kim, Minjoo Shin, Kyung Un Choi, Dong Soo Suh, Yun Hak Kim, Tae-Ho Hwang, Jae Ho Kim

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-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

15 citing papers in PubMed, 18 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

10 authors at 3 institutions in 1 country.

Seoyul LeeDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Wookyeom YangDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Dae Kyoung KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Hojun KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Minjoo ShinDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Kyung Un ChoiDepartment of Pathology, Pusan National University Hospital, Busan 49241, Republic of Korea.
Dong Soo SuhDepartment of Obstetrics and Gynecology, Pusan National University Hospital, Busan 49241, Republic of Korea.
Yun Hak KimDepartment of Anatomy and Department of Biomedical Informatics, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Tae-Ho HwangGene and Cell Therapy Research Center for Vessel-associated Diseases, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Jae Ho KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 50612, Republic of Korea.
Pusan National University · KRPusan National University Hospital · KRPusan National University Yangsan Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncolytic vaccinia virus (OVV) has been reported to induce cell death in various types of cancer; however, the oncolytic activity of OVV in drug-resistant ovarian cancer remains limited. In the present study, we established doxorubicin-resistant ovarian cancer cells (A2780-R) from the A2780 human ovarian cancer cell line. Both A2780 and A2780-R cells were infected with OVV to explore its anticancer effects. Interestingly, OVV-infected A2780-R cells showed reduced viral replication and cell death compared with A2780 cells, suggesting their resistance against OVV-induced oncolysis; to understand the mechanism underlying this resistance, we explored the involvement of protein kinases. Among protein kinase inhibitors, PD0325901, an MEK inhibitor, significantly augmented OVV replication and cell death in A2780-R cells. PD0325901 treatment increased the phosphorylation of STAT3 in A2780-R cells. Moreover, cryptotanshinone, a STAT3 inhibitor, abrogated PD0325901-stimulated OVV replication. Furthermore, trametinib, a clinically approved MEK inhibitor, increased OVV replication in A2780-R cells. Transcriptomic analysis showed that the MEK inhibitor promoted OVV replication via increasing STAT3 activation and downregulating the cytosolic DNA-sensing pathway. Combined treatment with OVV and trametinib attenuated A2780-R xenograft tumor growth. These results suggest that pharmacological inhibition of MEK reinforces the oncolytic efficacy of OVV in drug-resistant ovarian cancer.

Indexed as

cytosolic DNA sensingdoxorubicin-resistantMEKoncolytic vaccinia virusovarian cancerSTAT3virotherapy

Identifiers

PMID35592390
PMCPMC9096472
OpenAlexW4224316383

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.