FMNL3 Promotes Migration and Invasion of Breast Cancer Cells via Inhibiting Rad23B-Induced Ubiquitination of Twist1.

Breast cancer is a heterogeneous malignant tumor, and its high metastasis rate depends on the abnormal activation of cell dynamics. Formin-like protein 3 (FMNL3) plays an important role in the formation of various cytoskeletons that participate in cell movement. The objective of this study was to explore the function of FMNL3 in breast cancer progression and endeavor to reveal the molecular mechanism of this phenomenon.

Association between breastfeeding, mammographic density, and breast cancer risk: a review.

Background: Mammographic density has been associated with breast cancer risk, and is modulated by established breast cancer risk factors, such as reproductive and hormonal history, as well as lifestyle. Recent epidemiological and biological findings underscore the recognized benefits of breastfeeding in reducing breast cancer risk, especially for aggressive subtypes. Current research exploring the association among mammographic density, breastfeeding, and breast cancer is sparse.

Inhibition of ABI2 ubiquitination-dependent degradation suppresses TNBC cell growth via down-regulating PI3K/Akt signaling pathway.

Triple negative breast cancer (TNBC) is a type of cancer that lacks receptor expression and has complex molecular mechanisms. Recent evidence shows that the ubiquitin-protease system is closely related to TNBC. In this study, we obtain a key ubiquitination regulatory substrate-ABI2 protein by bioinformatics methods, which is also closely related to the survival and prognosis of TNBC.

GATA4 regulates the transcription of MMP9 to suppress the invasion and migration of breast cancer cells via HDAC1-mediated p65 deacetylation.

GATA-binding protein 4 (GATA4) is recognized for its significant roles in embryogenesis and various cancers. Through bioinformatics and clinical data, it appears that GATA4 plays a role in breast cancer development. Yet, the specific roles and mechanisms of GATA4 in breast cancer progression remain elusive.

α-Catenin acetylation is essential for its stability and blocks its tumor suppressor effects in breast cancer through Yap1.

α-Catenin plays a critical role in tissue integrity, repair, and embryonic development. However, the post-translational modifications of α-catenin and the correlative roles in regulating cancer progression remain unclear. Here, we report that α-catenin is acetylated by p300, and identify three acetylation sites, K45, K866, and K881.

KLF12 promotes the proliferation of breast cancer cells by reducing the transcription of p21 in a p53-dependent and p53-independent manner.

Breast cancer is the most common cancer affecting women worldwide. Many genes are involved in the development of breast cancer, including the Kruppel Like Factor 12 (KLF12) gene, which has been implicated in the development and progression of several cancers. However, the comprehensive regulatory network of KLF12 in breast cancer has not yet been fully elucidated.

Cryptochrome 2 acetylation attenuates its antiproliferative effect in breast cancer.

Breast cancer is the most commonly diagnosed cancer, and its global impact is increasing. Its onset and progression are influenced by multiple cues, one of which is the disruption of the internal circadian clock. Cryptochrome 2 (Cry2) genetic dysregulation may lead to the development of some diseases and even tumors.

USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination.

Purpose: Epithelial-to-mesenchymal transition (EMT) is an important cause of high mortality in breast cancer. Twist1 is one of the EMT transcription factors (EMT-TFs) with a noticeably short half-life, which is regulated by proteasome degradation pathways. Recent studies have found that USP13 stabilizes several specific oncogenic proteins.

Trend of disease burden and risk factors of breast cancer in developing countries and territories, from 1990 to 2019: Results from the Global Burden of Disease Study 2019.

Background: The incidence, mortality, burden of disability-adjusted life years (DALYs), and attributable risk factors of breast cancer vary significantly by country or region, particularly between developing and developed countries. This study aimed to analyze breast cancer development trends in developing countries based on the influence of the different sociodemographic indices (SDIs) and World Bank (WB) income-level disease data from 1990 to 2019.

Methods: Data on the annual incidence, mortality, DALY, years of life lost (YLL) prematurely, years lived with disability (YLD), and age-standardized rate (ASR) of breast cancer from 1990 to 2019 in different countries and territories were obtained from the 2019 Global Burden of Disease (GBD) Study.

The Role of PPARs in Breast Cancer.

Breast cancer is a malignant tumor with high morbidity and lethality. Its pathogenesis is related to the abnormal expression of many genes. The peroxisome proliferator-activated receptors (PPARs) are a class of ligand-dependent transcription factors in the nuclear receptor superfamily.

The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.

Small ubiquitin-like modifier (SUMO)ylation is a reversible post-translational modification that plays a crucial role in numerous aspects of cell physiology, including cell cycle regulation, DNA damage repair, and protein trafficking and turnover, which are of importance for cell homeostasis. Mechanistically, SUMOylation is a sequential multi-enzymatic process where SUMO E3 ligases recruit substrates and accelerate the transfer of SUMO onto targets, modulating their interactions, localization, activity, or stability. Accumulating evidence highlights the critical role of dysregulated SUMO E3 ligases in processes associated with the occurrence and development of cancers.

DACH1 inhibits breast cancer cell invasion and metastasis by down-regulating the transcription of matrix metalloproteinase 9.

Human Dachshund homolog 1 (DACH1) is usually defined as a tumor suppressor, which plays an influential role in tumor growth and metastasis in a variety of cancer cells. However, the underlying mechanisms in these process are not yet fully clarified. In this study, DACH1 inhibited the invasion and metastasis of breast cancer cells by decreasing MMP9 expression.

FBXL10 promotes EMT and metastasis of breast cancer cells via regulating the acetylation and transcriptional activity of SNAI1.

F-box and leucine-rich repeat protein 10 (FBXL10) has been reported to play a regulatory role in the initiation and development of breast cancer. Bioinformatics analyses revealed that FBXL10 may involve in the process of cytoskeleton organization. This research aimed to investigate the function of FBXL10 in epithelial-mesenchymal transition (EMT) and metastasis of breast cancer, and tried to reveal the molecular mechanism involved in this issue.

Codelivery of High-Molecular-Weight Poly-porphyrins and HIF-1α Inhibitors for Synergistic Anticancer Therapy.

Photodynamic therapy (PDT) is showing great potential in the treatment of cancer diseases, and photosensitizers play crucial roles in absorbing the energy of light and generating reactive oxygen species (ROS) during PDT. Most of the photosensitizers bearing macrocyclic structures have strong hydrophobicity and suffer from the π-π interaction and undesired aggregation caused quenching (ACQ), which severely limit the PDT efficacy. Moreover, the continuous oxygen consumption during PDT also leads to the upregulated expression of hypoxia-inducible factor-1α (HIF-1α), which can aggravate the growth of tumors.

Linear and high-molecular-weight poly-porphyrins for efficient photodynamic therapy.

Photodynamic therapy (PDT) holds great potential in cancer treatment due to the advantages of non-invasiveness, negligible side-effect, and high spatiotemporal selectivity. Porphyrin is the most widely used photosensitizer in clinical treatment. However, its PDT efficacy is always limited by the undesired aggregation caused quenching (ACQ) effect originating from the planar and rigid structure.

Twisted BODIPY derivative: intersystem crossing, electron spin polarization and application as a novel photodynamic therapy reagent.

The photophysical properties of a heavy atom-free BODIPY derivative with a twisted π-conjugated framework were studied. Efficient intersystem crossing (ISC quantum yield: 56%) and an exceptionally long-lived triplet state were observed (4.5 ms in solid polymer film matrix and 197.

Acetylation of ELF5 suppresses breast cancer progression by promoting its degradation and targeting CCND1.

E74-like ETS transcription factor 5 (ELF5) is involved in a wide spectrum of biological processes, e.g., mammogenesis and tumor progression.

The role of post-translational modifications in the regulation of MCL1.

Apoptosis is an evolutionarily conserved form of programed cell death (PCD) that has a vital effect on early embryonic development, tissue homeostasis and clearance of damaged cells. Dysregulation of apoptosis can lead to many diseases, such as Alzheimer's disease, cancer, AIDS and heart disease. The anti-apoptotic protein MCL1, a member of the BCL2 family, plays important roles in these physiological and pathological processes.

FBXL10 promotes ERRα protein stability and proliferation of breast cancer cells by enhancing the mono-ubiquitylation of ERRα.

The underlying mechanism of orphan nuclear receptor estrogen-related receptor α (ERRα) in breast cancer was investigated by identifying its interaction partners using mass spectrometry. F-box and leucine-rich repeat protein 10 (FBXL10), which modulates various physiological processes, may interact with ERRα in breast cancer. Here, we investigated the interaction between FBXL10 and ERRα, and their protein expression and correlation in breast cancer.

TIMELESS inhibits breast cancer cell invasion and metastasis by down-regulating the expression of MMP9.

Breast cancer is the first killer leading to female death, and tumor metastasis is one of the important factors leading to the death of patients, but the specific mechanism of breast cancer metastasis is not very clear at present. Our study showed that overexpression of TIMELESS could significantly inhibit the invasion and metastasis of breast cancer cells ZR-75-30 and the assembly of F-actin protein. On the contrary, knockdown of TIMELESS promoted the invasion and metastasis of breast cancer cells.