Evidence map›Paper›PMID 33575078›Full record

ArticleAmerican journal of cancer research2021

CDCA8, targeted by MYBL2, promotes malignant progression and olaparib insensitivity in ovarian cancer.

Gonghua Qi, Chenyi Zhang, Hanlin Ma, Yingwei Li, Jiali Peng, Jingying Chen, Beihua Kong

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  8. Review
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  10. Delivery of SIRT1 by cancer-associated adipocyte-derived extracellular vesicles regulates immune response and tumorigenesis of ovarian cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  11. Article
  12. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  13. Article
  14. Article
  15. KNTC1 as a putative tumor oncogene in pancreatic cancer.Journal of cancer research and clinical oncology · 2023
    Article
  16. 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

7 authors at 1 institution in 1 country.

Gonghua QiDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Chenyi ZhangDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Hanlin MaDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Yingwei LiDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Jiali PengDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Jingying ChenDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Beihua KongDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University Jinan 250012, China.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecologic malignancy. Poly (ADP-ribose) polymerase inhibitors (PARPi) are effective in treating ovarian cancer. However, cancer cell insensitivity and resistance remain challenges. Determination of the exact chemoresistance mechanisms and potential targeted therapies is urgent. CDCA8 (cell division cycle associated 8) participates in the tumorigenesis of various cancers; however, the exact biological function of CDCA8 in ovarian cancer remains obscure. Here, we found that CDCA8 was overexpressed in ovarian cancer and that high expression of CDCA8 promoted the proliferation of ovarian cancer cells in vitro and in vivo. Moreover, silencing of CDCA8 sensitized ovarian cancer cells to olaparib and cisplatin by inducing G2/M arrest, accelerating apoptosis, increasing DNA damage and interfering with RAD51 accumulation in vitro. In addition, MYBL2 (MYB proto-oncogene-like 2), identified as an upstream transcription factor of CDCA8, was positively correlated with the expression level of CDCA8 in ovarian cancer. Finally, MYBL2 enhanced the aggressive characteristics of ovarian cancer cells by regulating CDCA8. In conclusion, high CDCA8 expression was involved in the tumorigenesis, aggressiveness and chemoresistance of ovarian cancer. CDCA8 silencing combined with olaparib treatment might lead to substantial progress in ovarian cancer targeted therapy.

Indexed as

CDCA8G2/M arresthomologous recombination-mediated repairolaparibOvarian cancer

Identifiers

PMID33575078
PMCPMC7868764
OpenAlexW3127795805

What OpenQuestion holds

Textmetadata
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.