ArticleJournal of experimental & clinical cancer research : CR2017
The oncogenic Golgi phosphoprotein 3 like overexpression is associated with cisplatin resistance in ovarian carcinoma and activating the NF-κB signaling pathway.
Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.
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.
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.
Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- A genome-wide association study using HapMap cell lines reveals modulators of cellular response to cyclophosphamide.Future oncology (London, England) · 2025Article
- RNF149 confers cisplatin resistance in esophageal squamous cell carcinoma via destabilization of PHLPP2 and activating PI3K/AKT signalling.Medical oncology (Northwood, London, England) · 2023Article
- Article
- Family with sequence similarity 46 member a confers chemo-resistance to ovarian carcinoma via TGF-β/Smad2 signaling.Bioengineered · 2022Article
- Independent duplications of the Golgi phosphoprotein 3 oncogene in birds.Scientific reports · 2021Article
- The miR-1185-2-3p-GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1.Journal of experimental & clinical cancer research : CR · 2021Article
- Research Progress in Prognostic Factors and Biomarkers of Ovarian Cancer.Journal of Cancer · 2021Review
- CCL20 Promotes Ovarian Cancer Chemotherapy Resistance by Regulating ABCB1 Expression.Cell structure and function · 2019Article
- Article
- Overexpression of kinesin family member 20A is associated with unfavorable clinical outcome and tumor progression in epithelial ovarian cancer.Cancer management and research · 2018Article
Corrections and comments
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemo-resistance is a leading cause of tumor relapse and treatment failure in patients with ovarian cancer. The identification of effective strategies to overcome drug resistance will have a significant clinical impact on the disease.
methodsThe protein and mRNA expression of GOLPH3L in ovarian cancer cell lines and patient tissues were determined using Real-time PCR and Western blot, respectively. 177 human ovarian cancer tissue samples were analyzed by IHC to investigate the association between GOLPH3L expression and the clinicopathological characteristics of ovarian cancer patients. Functional assays, such as MTT, FACS, and Tunel assay used to determine the oncogenic role of GOLPH3L in human ovarian cancer progression. Furthermore, western blotting and luciferase assay were used to determine the mechanism of GOLPH3L promotes chemoresistance in ovarian cancer cells.
resultsThe expression of GOLPH3L was markedly upregulated in ovarian cancer cell lines and tissues, and high GOLPH3L expression was associated with an aggressive phenotype and poor prognosis with ovarian cancer patients. GOLPH3L overexpression confers CDDP resistance on ovarian cancer cells; however, inhibition of GOLPH3L sensitized ovarian cancer cell lines to CDDP cytotoxicity both in vitro and in vivo. Additionally, GOLPH3L upregulated the levels of nuclear p65 and phosphorylated inhibitor of nuclear factor Kappa-B kinase-β and IκBα, thereby activating canonical nuclear factor-κB (NF-κB) signaling.
conclusionsOur findings suggest that GOLPH3L is a potential therapeutic target for the treatment of ovarian cancer: targeting GOLPH3L signaling may represent a promising strategy to enhance platinum response in patients with chemoresistant ovarian cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.