Background: Sustaining proliferation is the most fundamental step for breast cancer tumor genesis. Accelerated proliferation is usually linked to the uncontrolled cell cycle. However, the internal and external factors linked to the activation of breast cancer cell cycle are still to be investigated.

Methods: quantitative PCR (qPCR) and Western blotting assay were used to detect the expression of potassium channel tetramerization domain containing 12 (KCTD12) in breast cancer. MTT and colony formation assays were performed to evaluate the effect of KCTD12 on cell proliferation of breast cancer. Anchorage-independent growth assay was used to examine the in vitro tumorigenesis of breast cancer cells. Flow cytometry assay, qPCR, and Western blotting were used to investigate the detailed mechanisms of KCTD12 on breast cancer progression.

Results: Herein, the result showed that the level of KCTD12 is significantly decreased in breast cancer tissues and cells, and lower level of KCTD12 predicts poorer survival for patients with breast cancer. Further cell function tests illustrated that downregulation of KCTD12 significantly promotes cell proliferation and in vitro tumor genesis. Besides, molecular biologic experiments showed that downregulation of KCTD12 can enhance the G1/S transition through activating the AKT/FOXO1 signaling.

Conclusion: Our study inferred that downregulation of KCTD12 can be a novel factor for poor prognosis in breast cancer.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439418PMC
http://dx.doi.org/10.1002/jcla.23315DOI Listing

Publication Analysis

Top Keywords

breast cancer
40
cancer cell
12
downregulation kctd12
12
breast
10
cancer
10
kctd12
9
kctd12 promotes
8
g1/s transition
8
activating akt/foxo1
8
tumor genesis
8

Similar Publications

This study investigates the potential treatment of breast cancer utilizing Gentiana robusta King ex Hook. f. (QJ) through an integrated approach involving network pharmacology, molecular docking, and molecular dynamics simulation.

View Article and Find Full Text PDF

Early prediction of patient responses to neoadjuvant chemotherapy (NACT) is essential for the precision treatment of early breast cancer (EBC). Therefore, this study aims to noninvasively and early predict pathological complete response (pCR). We used dynamic ultrasound (US) imaging changes acquired during NACT, along with clinicopathological features, to create a nomogram and construct a machine learning model.

View Article and Find Full Text PDF

Metaplastic breast cancer (MpBC) is a highly chemoresistant subtype of breast cancer with no standardized therapy options. A clinical study in anthracycline-refractory MpBC patients suggested that nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine (L-NMMA) may augment anti-tumor efficacy of taxane. We report that NOS blockade potentiated response of human MpBC cell lines and tumors to phosphoinositide 3-kinase (PI3K) inhibitor alpelisib and taxane.

View Article and Find Full Text PDF

the evolution of axillary management in breast cancer has witnessed significant changes in recent decades, leading to an overall reduction in surgical interventions. There have been notable shifts in practice, aiming to minimize morbidity while maintaining oncologic outcomes and accurate staging for newly diagnosed breast cancer patients. These advancements have been facilitated by the improved efficacy of adjuvant therapies.

View Article and Find Full Text PDF

the axillary reverse mapping (ARM) procedure aims to preserve the lymphatic drainage structures of the upper extremity during axillary surgery for breast cancer, thereby reducing the risk of lymphedema in the upper limb. Material and this prospective study included 57 patients with breast cancer who underwent SLNB and ARM. The sentinel lymph node (SLN) was identified using a radioactive tracer.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!