Evidence map›Paper›PMID 39001931›Full record

ArticleMolecular biology reports2024

Suppression of CTC1 inhibits hepatocellular carcinoma cell growth and enhances RHPS4 cytotoxicity.

Arda Kipcak, Sila Sezan, Ozum Karpat, Ezgi Kaya, Sude Baylan, Ece Sariyar, Cihangir Yandim, Zeynep Firtina Karagonlar

Abstract read
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Article in Molecular biology reports, 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. Article
  2. Organoids and spheroids: advancedFrontiers in cell and developmental biology · 2024
    Review
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

8 authors.

Arda Kipcak *Department of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey.
Sila Sezan *Division of Bioengineering, Graduate School, İzmir University of Economics, Sakarya Cad, İzmir, Turkey.
Ozum KarpatDepartment of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey.
Ezgi KayaDepartment of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey.
Sude BaylanDepartment of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey.
Ece SariyarDivision of Bioengineering, Graduate School, İzmir University of Economics, Sakarya Cad, İzmir, Turkey.
Cihangir YandimDepartment of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey.
Zeynep Firtina KaragonlarDepartment of Genetics and Bioengineering, Izmir University of Economics, Sakarya Cad, İzmir, Turkey. zeynep.firtina@ieu.edu.tr.

Funding

Türkiye Bilimsel ve Teknolojik Araştırma Kurumu 222S568
6 · The paper itself

Abstract

backgroundAlthough DNA repair mechanisms function to maintain genomic integrity, in cancer cells these mechanisms may negatively affect treatment efficiency. The strategy of targeting cancer cells via inhibiting DNA damage repair has been successfully used in breast and ovarian cancer using PARP inhibitors. Unfortunately, such strategies have not yet yielded results in liver cancer. Hepatocellular carcinoma (HCC), the most common type of liver cancer, is a treatment-resistant malignancy. Despite the development of guided therapies, treatment regimens for advanced HCC patients still fall short of the current need and significant problems such as cancer relapse with resistance still exist. In this paper, we targeted telomeric replication protein CTC1, which is responsible for telomere maintenance.

methodsCTC expression was analyzed using tumor and matched-tissue RNA-sequencing data from TCGA and GTEx. In HCC cell lines, q-RT-PCR and Western blotting were used to detect CTC1 expression. The knock-down of CTC1 was achieved using lentiviral plasmids. The effects of CTC1 silencing on HCC cells were analyzed by flow cytometry, MTT, spheroid and colony formation assays.

resultsCTC1 is significantly downregulated in HCC tumor samples. However, CTC1 protein levels were higher in sorafenib-resistant cell lines compared to the parental groups. CTC1 inhibition reduced cell proliferation in sorafenib-resistant HCC cell lines and diminished their spheroid and colony forming capacities. Moreover, these cells were more sensitive to single and combined drug treatment with G4 stabilizer RHPS4 and sorafenib.

conclusionOur results suggest that targeting CTC1 might be a viable option for combinational therapies designed for sorafenib resistant HCC patients.

Indexed as

Carcinoma, HepatocellularCell ProliferationDrug Resistance, NeoplasmLiver NeoplasmsSorafenibCell Line, TumorGene Expression Regulation, NeoplasticHumansTelomere-Binding ProteinsCtc1 protein, humanSorafenibTelomere-Binding ProteinsCTC1G-quadruplex DNAHepatocellular carcinoma HCCLiver cancerRHSP4

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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.