Evidence map›Paper›PMID 39710372›Full record

ArticleCancer reports (Hoboken, N.J.)2024

Forced Vasohibin-1 Expression Increases Paclitaxel Sensitivity of Ovarian Cancer by Inhibiting Microtubule Activity.

Takahiro Koyanagi, Yasushi Saga, Yoshifumi Takahashi, Kohei Tamura, Suzuyo Takahashi, Akiyo Taneichi, Yuji Takei, Hiroaki Mizukami, Hiroyuki Fujiwara

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Takahiro KoyanagiDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.ORCID 0000-0001-8669-4880
Yasushi SagaDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Yoshifumi TakahashiDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Kohei TamuraDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Suzuyo TakahashiDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Akiyo TaneichiDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Yuji TakeiDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Hiroaki MizukamiDivision of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Hiroyuki FujiwaraDepartment of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Funding

Ministry of Education, Culture, Sports, Science and Technology of Japan 17K11294Ministry of Education, Culture, Sports, Science and Technology of Japan 19K18702Ministry of Education, Culture, Sports, Science and Technology of Japan 20K09627Ministry of Education, Culture, Sports, Science and Technology of Japan 22K09551
6 · The paper itself

Abstract

backgroundVasohibin-1 (VASH1), an angiogenic inhibitor, exhibits tubulin carboxypeptidase activity, which is involved in microtubule functions. Paclitaxel, the core chemotherapeutic agent for ovarian cancer chemotherapy, has a point of action on microtubules and may interact with VASH1.

aimsTo examine the influence of VASH1 on intracellular tubulin detyrosination status, cyclin B1 expression, and paclitaxel chemosensitivity using VASH1-overexpressing ovarian cancer cell lines. METHODS AND

resultsGene-transfected human ovarian cancer cell lines were subjected to western blot analysis. Western blot analysis of VASH1-overexpressing ovarian cancer cells revealed upregulated expression of detyrosinated tubulin and cyclin B1 compared with control cells. By WST-1 assay, paclitaxel chemosensitivity of VASH1-overexpressing ovarian cancer cells was markedly enhanced compared with that of control cells, whereas there was no significant difference in chemosensitivity to cisplatin. The forced expression of VASH1 enhanced tubulin carboxypeptidase activity and increased cyclin B1 expression, resulting in augmented paclitaxel chemosensitivity in ovarian cancer cells.

conclusionOvarian cancer treatment strategies targeting VASH1 can potentiate the effects of conventional chemotherapy by inhibiting angiogenesis and regulating microtubule activity.

Indexed as

Cell Cycle ProteinsCyclin B1MicrotubulesOvarian NeoplasmsPaclitaxelAntineoplastic Agents, PhytogenicCarboxypeptidasesCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansTubulinAntineoplastic Agents, PhytogenicCarboxypeptidasesCCNB1 protein, humanCell Cycle ProteinsCyclin B1PaclitaxelTubulinVASH1 protein, humancell cycledetyrosinated tubulinovarian cancerpaclitaxelvasohibin‐1

Identifiers

PMID39710372
PMCPMC11663491

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.