Evidence map›Paper›PMID 26335100›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2015

The carboxy-terminal domain of connexin 43 (CT-Cx43) modulates the expression of p53 by altering miR-125b expression in low-grade human breast cancers.

Raihana Maqbool, Rabiya Rashid, Rehana Ismail, Saif Niaz, Nisar Ahmad Chowdri, Mahboob Ul Hussain

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Article in Cellular oncology (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 23 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

6 authors at 2 institutions in 1 country.

Raihana MaqboolDepartment of Biotechnology, University of Kashmir, Srinagar, 190006, India.
Rabiya RashidDepartment of Biotechnology, University of Kashmir, Srinagar, 190006, India.
Rehana IsmailDepartment of Biotechnology, University of Kashmir, Srinagar, 190006, India.
Saif NiazDepartment of Biotechnology, University of Kashmir, Srinagar, 190006, India.
Nisar Ahmad ChowdriDepartment of General and Minimal Invasive Surgery, SKIMS, Srinagar, Soura, India.
Mahboob Ul HussainDepartment of Biotechnology, University of Kashmir, Srinagar, 190006, India. mahboob@kashmiruniversity.ac.in.
University of Kashmir · INSher-i-Kashmir Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeConnexin 43 (Cx43) is a widely expressed gap junction protein. It can also regulate various gap-junction independent processes, including cellular proliferation. The latter regulatory functions have been attributed to its carboxy-terminal domain, CT-Cx43. CT-Cx43 has been found to be expressed independent of full-length Cx43 in various cell types. Its nuclear localization has additionally raised the possibility that it may regulate the expression of particular genes, including miRNAs, known play a role in the regulation of cellular proliferation. Here, we set out to uncover the molecular mechanism(s) underlying CT-Cx43 mediated gene (de-)regulation in human breast cancer.

methodsWestern blotting and quantitative real time PCR were carried to assess the expression of CT-Cx43 and miR-125b in a panel of 60 primary human breast cancer tissues and its paired normal adjacent tissues. In addition, CT-Cx43 was exogenously expressed in the breast cancer-derived cell line MCF-7 and its effect on the expression of miR-125b and its downstream target p53 were evaluated, as well as its effect on cellular proliferation and death using MTT and LDH assays, respectively.

resultsWe found that CT-Cx43, but not full-length Cx43, was down-regulated in low grade human breast cancers. In addition, we found that the tumor suppressor protein p53 exhibited a decreased expression in the CT-Cx43 down-regulated samples. Interestingly, we found that miR-125b, a negative regulator of p53, exhibited an inverse expression relationship with CT-Cx43 in the breast cancer samples tested. This inverse relationship was confirmed by exogenous expression of CT-Cx43 in MCF-7 cells. In addition, we found that CT-Cx43 up-regulation and subsequent miR-125b down-regulation resulted in a decreased proliferation of MCF-7 cells.

conclusionsOur data suggest a mechanism by which CT-Cx43 may regulate cell proliferation. Targeting of CT-Cx43 and/or miR-125b may be instrumental for therapeutic intervention in human breast cancer.

Indexed as

Blotting, WesternBreast NeoplasmsConnexin 43FemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsNeoplasm GradingReal-Time Polymerase Chain ReactionTransfectionTumor Suppressor Protein p53Connexin 43GJA1 protein, humanMicroRNAsMIRN125 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53Breast cancerConnexin43miR-125bp53

Identifiers

PMID26335100
PMCPMC13004188
OpenAlexW1769232711

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Registered trials

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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.