The long non‑coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. However, the mechanism by which NEAT1 regulates breast cancer progression is not well elucidated. In the present study, NEAT1 and microRNA‑124 (miR‑124) levels were detected by reverse transcription‑quantitative PCR in breast cancer tissues and cell lines. STAT3 protein levels were detected by western blot analysis. Cell proliferation and cell cycle distribution were determined using MTT and colony formation assays, and flow cytometry, respectively. The results demonstrated that NEAT1 and STAT3 expression levels were increased in breast cancer tissues compared with normal breast tissues, whereas miR‑124 expression was significantly decreased. Functional analyses revealed that NEAT1 promoted cell proliferation and cell cycle progression in breast cancer cells. Additionally, NEAT1 and STAT3 expression levels were negatively correlated with miR‑124 levels in breast cancer tissues. A direct interaction between miR‑124, and NEAT1 and STAT3, was predicted by bioinformatics analysis and confirmed using a luciferase activity assay. NEAT1 overexpression markedly increased STAT3 protein expression levels, and this effect was reversed by miR‑124 overexpression in breast cancer cells. Furthermore, miR‑124 overexpression partially attenuated the effects of NEAT1 on breast cancer cell proliferation and cell cycle progression. The inhibitory effects of miR‑124 overexpression on the proliferation rate and cell cycle progression were abolished by STAT3 overexpression. In turn, STAT3 silencing inhibited NEAT1 transcription in breast cancer cells. In summary, the present findings revealed that NEAT1 and STAT3 formed a feedback loop via sponging miR‑124 to promote breast cancer progression.
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http://dx.doi.org/10.3892/ijo.2019.4841 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Pharmacology, School of Pharmacy, China Medical University, Shenyang, 110122, China.
Hydrogen sulfide (HS)-mediated protein S-sulfhydration has been shown to play critical roles in several diseases. Tumor-associated macrophages (TAMs) are the predominant population of immune cells present within solid tumor tissues, and they function to restrict antitumor immunity. However, no previous study has investigated the role of protein S-sulfhydration in TAM reprogramming in breast cancer (BC).
View Article and Find Full Text PDFAnn Surg Oncol
January 2025
Department of Surgery, Duke University Medical Center, Durham, NC, USA.
Background: Bilateral risk-reducing mastectomies (RRMs) have been proven to decrease the risk of breast cancer in patients at high risk owing to family history or having pathogenic genetic mutations. However, few resources with consolidated data have detailed the patient experience following surgery. This systematic review features patient-reported outcomes for patients with no breast cancer history in the year after their bilateral RRM.
View Article and Find Full Text PDFAnn Surg Oncol
January 2025
Department of Plastic and Reconstructive Surgery, The Ohio State University, Columbus, OH, USA.
Cancer Causes Control
January 2025
Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, State University of New York at Buffalo, 265 Farber Hall, Buffalo, NY, 14214, USA.
Purpose: Historical redlining, a 1930s-era form of residential segregation and proxy of structural racism, has been associated with breast cancer risk, stage, and survival, but research is lacking on how known present-day breast cancer risk factors are related to historical redlining. We aimed to describe the clustering of present-day neighborhood-level breast cancer risk factors with historical redlining and evaluate geographic patterning across the US.
Methods: This ecologic study included US neighborhoods (census tracts) with Home Owners' Loan Corporation (HOLC) grades, defined as having a score in the Historic Redlining Score dataset; 2019 Population Level Analysis and Community EStimates (PLACES) data; and 2014-2016 Environmental Justice Index (EJI) data.
Apoptosis
January 2025
Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer-associated fibroblasts (CAFs) significantly influence tumor progression and therapeutic resistance in colorectal cancer (CRC). However, the distributions and functions of CAF subpopulations vary across the four consensus molecular subtypes (CMSs) of CRC. This study performed single-cell RNA and bulk RNA sequencing and revealed that myofibroblast-like CAFs (myCAFs), tumor-like CAFs (tCAFs), inflammatory CAFs (iCAFs), CXCL14CAFs, and MTCAFs are notably enriched in CMS4 compared with other CMSs of CRC.
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