Evidence map›Paper›PMID 27313771›Full record

ArticleOncology letters2016

Knockdown of cathepsin L sensitizes ovarian cancer cells to chemotherapy.

Hongmei Zhang, Luosheng Zhang, Lixia Wei, Xingwang Gao, L I Tang, Wei Gong, N A Min, L I Zhang, Yawei Yuan

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 43 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

9 authors at 2 institutions in 1 country.

Hongmei ZhangDepartment of Radiation Oncology, Nangfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China; Department of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
Luosheng ZhangDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
Lixia WeiDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
Xingwang GaoDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
L I TangDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
Wei GongDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
N A MinDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
L I ZhangDepartment of Oncology, The 458th Hospital of the People's Liberation Army, Guangzhou, Guangdong 510602, P.R. China.
Yawei YuanDepartment of Radiation Oncology, Nangfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
458th Hospital PLA · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is a leading gynecological malignancy associated with high mortality. The development of acquired drug resistance is the primary cause of chemotherapy failure in the treatment of ovarian cancer. To examine the mechanism underlying paclitaxel resistance in ovarian cancer and attempt to reverse it, the present study induced a TAX-resistant ovarian cancer cell line, SKOV3/TAX. Cathepsin L (CTSL) has been found to be overexpressed in ovarian cancer. The aim of the present study was to investigate the possible involvement of CTSL in the development of TAX resistance in ovarian cancer. CTSL expression was knocked down in SKOV3 ovarian cancer cells and their phenotypic changes were analyzed. The effects of silenced CTSL on the resistant cell line were investigated by proliferation and apoptosis analysis compared with control SKOV3 cells. CTSL was more highly expressed in SKOV3/TAX cells compared with SKOV3 cells. Paclitaxel treatment downregulated the expression of CTSL in SKOV-3 but not in the paclitaxel-resistant SKOV3/TAX cells. CTSL small hairpin RNA (shRNA) knockdown significantly potentiated apoptosis induced by paclitaxel compared with SKOV3/TAX cells transfected with control shRNA, suggesting that CTSL contributes to paclitaxel resistance in ovarian cancer cells and that CTSL silencing can enhance paclitaxel-mediated cell apoptosis. Thus, CTSL should be explored as a candidate of therapeutic target for modulating paclitaxel sensitivity in ovarian cancer.

Indexed as

apoptosiscathepsin Lchemoresistanceovarian cancerpaclitaxelproliferationSKOV3/TAX cells

Identifiers

PMID27313771
PMCPMC4888267
OpenAlexW2342469494

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.