C1orf63 silencing affects breast cancer cell proliferation, apoptosis, and cycle distribution by NF-κB signaling pathway.

Lijun Zhang, Hua Zhang, Yaqiong Li, Lingcheng Wang

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Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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4 authors at 2 institutions in 1 country.

Lijun ZhangDepartment of Breast Surgery, The First People's Hospital of Jingzhou Jingzhou, Hubei Province, China.

Hua ZhangDepartment of General Surgery Ward 3, Affiliated Taihe Hospital of Hubei University of Medicine Shiyan, Hubei Province, China.

Yaqiong LiDepartment of Thyroid, Breast and Vascular Surgery, Renmin Hospital, Hubei University of Medicine Shiyan, Hubei Province, China.

Lingcheng WangDepartment of Thyroid, Breast and Vascular Surgery, Renmin Hospital, Hubei University of Medicine Shiyan, Hubei Province, China.

Hubei University of Medicine · CNFirst People's Hospital of Jingzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the effect of C1orf63 on breast cancer cell (BCC) proliferation, apoptosis, and cycle distribution and related mechanisms.

methodsThe expression of C1orf63 was interfered with in BCC line MCF and cells were divided into a C1orf63 overexpression group, C1orf63 silence group, blank group, and empty group. The mRNA expression of C1orf63 and the proliferation, apoptosis, and cycle distribution of BCCs were detected. The mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, Bcl-2, and Bax) in each group were also detected.

resultsThere was no significant difference between the blank group and empty group in the expression level of C1orf63 mRNA, cell proliferation rate, apoptosis rate, cell distribution rate, or mRNA expression levels of the NF-κB signaling pathway factors (all P>0.05). The expression levels of C1orf63 mRNA in the C1orf63 silenced group were lower than those in the other two groups (P<0.05). The cell proliferation rate, cell distribution in S phase and G2/M phase, and the mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, and Bcl-2) in the C1orf63 silenced group at each time point were lower than those in the other two groups (all P<0.05). The apoptosis rate, cells in G1 phase, and the Bax mRNA expression level in C1orf63 silenced group at each time point were higher than those in the other two groups (all P<0.05).

conclusionDown-regulation of C1orf63 acts on the NF-κB signaling pathway to regulate the expression of p-IκBα, CyclinD1, and CDK4, so as to inhibit BCC proliferation, promote cell apoptosis, and block the cell cycle.

Indexed as

apoptosisbreast cancer cellC1orf63cell cycleproliferation

Identifiers

PMID34017419

PMCPMC8129316

OpenAlexW3163570640

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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.