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2022 ◽  
Vol 20 (6) ◽  
pp. 41-54
Author(s):  
N. A. Smetannikova ◽  
M. A. Abdurashitov ◽  
A. G. Akishev ◽  
P. I. Pozdnyakov ◽  
E. V. Dubinin ◽  
...  

Hypermethylation of the RcgY sites is shown for many cancer diseases. such aberrant methylation, suppressing the gene activity, occurs at early stages of carcinogenesis. Recently, using glad-pcR assay, we have detected aberrantly methylated RcgY sites, which can be considered to be epigenetic markers of colorectal, lung, and gastric cancers. in breast cancer, methylation of the regulatory regions of ALX4, BMP2, CCND2, CDH13, CDX1, FOXA1, GALR1, GATA5, GREM1, HIC1, HMX2, HS3ST2, HOXC10, ICAM5, LAMA1, RARB, RASSF1A, RUNX3, RXRG, RYR2, SFRP2, SOX17, TERT, and ZNF613 tumor-suppressor genes is reported. in the present work, we determined aberrantly methylated RcgY sites in the regulatory regions of these genes in dNa preparations from breast cancer tissues. the study of dNa samples from 30 tumor and 22 normal mammary tissue samples demonstrates a high diagnostic potential of selected R(5mc)gY sites in regulatory regions of CCND2, BMP2, GALR1, SOX17, HMX2, and HS3ST2 genes with total index of sensitivity and specificity for R(5mc)gY detection in tumor dNa 90.0 % and 100.0 %, respectively.


2022 ◽  
Vol 21 (1) ◽  
pp. 129-141
Author(s):  
Rayudika Aprilia Patindra Purba ◽  
Siwaporn Paengkoum ◽  
Chalermpon Yuangklang ◽  
Pramote Paengkoum ◽  
Abdelfattah Zeidan Mohamed Salem ◽  
...  

2021 ◽  
Author(s):  
Tzu-Yu Feng ◽  
Francesca N Azar ◽  
Claire B Rosean ◽  
Mitchell T McGinty ◽  
Audrey M Putelo ◽  
...  

Establishing commensal dysbiosis, defined as an inflammatory gut microbiome with low biodiversity, prior to breast tumor initiation, enhances early dissemination of hormone-receptor positive (HR+) mammary tumor cells. Here, we sought to define mammary tissue mediators of dysbiosis-induced tumor dissemination. We found that commensal dysbiosis increased both the frequency and profibrogenicity of mast cells in the mammary tissue, a phenotypic change that persisted after tumor implantation. Fibroblast activation and tissue remodeling associate with enhanced breast tumor metastasis. We employed pharmacological and adoptive transfer approaches to demonstrate that mammary tissue mast cells from dysbiotic animals enhances dissemination of HR+ tumor cells. Collagen levels in mammary tissues from HR+ breast cancer patients correlated with mast cell abundance, suggesting clinical relevance of mast cell-mediated fibroblast activation. Together, these data demonstrate that a gut-mast cell axis exists that induces fibroblast activation and orchestrates early dissemination of HR+ breast tumors.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Murat Erdem ◽  
İbrahim Ozgul ◽  
Didem Naz Dioken ◽  
Irmak Gurcuoglu ◽  
Sezen Guntekin Ergun ◽  
...  

AbstractRoles of HNRNPA1 are beginning to emerge in cancers; however, mechanisms causing deregulation of HNRNPA1 function remain elusive. Here, we describe an isoform switch between the 3′-UTR isoforms of HNRNPA1 in breast cancers. We show that the dominantly expressed isoform in mammary tissue has a short half-life. In breast cancers, this isoform is downregulated in favor of a stable isoform. The stable isoform is expressed more in breast cancers, and more HNRNPA1 protein is synthesized from this isoform. High HNRNPA1 protein levels correlate with poor survival in patients. In support of this, silencing of HNRNPA1 causes a reversal in neoplastic phenotypes, including proliferation, clonogenic potential, migration, and invasion. In addition, silencing of HNRNPA1 results in the downregulation of microRNAs that map to intragenic regions. Among these miRNAs, miR-21 is known for its transcriptional upregulation in breast and numerous other cancers. Altogether, the cancer-specific isoform switch we describe here for HNRNPA1 emphasizes the need to study gene expression at the isoform level in cancers to identify novel cases of oncogene activation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mie Naruse ◽  
Rikako Ishigamori ◽  
Toshio Imai

Here, we report a model system using in vitro 7,12-dimethylbenz[a]anthracene (DMBA; 0.6 μM)-treated mammary tissue-derived organoids generated from heterozygous BALB/c-Trp53 knockout mice to induce tumors after injection into the nude mouse subcutis. In parallel, a single oral dose of DMBA (50 mg/kg bodyweight) to the same murine strain induced mammary adenocarcinomas, characterized by biphasic structures differentiated into luminal and myoepithelial lineages and frequent Hras mutations at codon 61. In the present study, the genetic and histological characteristics of DMBA-induced tumors in the organoid-based model were evaluated to validate its similarities to the in vivo study. The organoid-derived tumors were low-grade adenocarcinomas composed of luminal and basal/myoepithelial cells. When the organoid-derived carcinomas were passaged to other nude mice, they partly progressed to squamous cell carcinomas (SCCs). Whole exome sequencing revealed no mutations at Hras codon 61 in the organoid-derived tumors. However, various mutations were detected in other genes such as Tusc3 and Tgfbr2, which have been reported as cancer-associated or homeostatic squamous cell genes. The most common mutational pattern observed in these genes were the G:C to T:A transversions and G:C to A:T transitions, which are not typical of the mutations caused by DMBA treatment. In conclusion, DMBA exhibited carcinogenicity in the both the ex vivo and in vivo mammary carcinogenesis models, albeit with distinct histological and genetical alterations. Further studies are needed to clarify whether organoid-based carcinogenesis models generated following chemical treatment in vitro could be applied to the clarification of the novel mode of action of chemical carcinogenesis.


2021 ◽  
Vol 2 (6) ◽  
Author(s):  
Angeles C. Tecalco-Cruz ◽  
Jesús Zepeda-Cervantes ◽  
Josué O. Ramírez-Jarquín ◽  
Alberto Rojas-Ochoa

Breast cancer (BC) is a highly heterogeneous neoplasm of the mammary tissue, causing the deaths of a large number of women worldwide. Nearly 70% and 20% of BC cases are estrogen receptor alpha positive (ERα+) and human epidermal growth factor receptor 2-positive (HER2+), respectively; therefore, ER and HER2 targeted therapies have been employed in BC treatment. However, resistance to these therapies has been reported, indicating a need for developing novel therapeutic strategies. Proteolysis-targeting chimeras (PROTACs) are new, promising therapeutic tools designed with a bimodular structure: one module allows specific binding to target proteins, and the other module allows efficient degradation of these target proteins. In this paper, PROTACs and their potential in controlling the progression of ERα and HER2+ BC are discussed.


2021 ◽  
Vol 28 (11) ◽  
pp. 715-730
Author(s):  
Thalles Fernando Rocha Ruiz ◽  
Simone J Colleta ◽  
Ellen C R Leonel ◽  
Sebastião Roberto Taboga

Compounds that trigger breast cancer onset and establishment are of great interest in biological research. Endocrine disruptors are relevant because they initiate carcinogenesis by changing endocrine pathways. Bisphenol A (BPA), as a ubiquitous xenoestrogen, is largely associated with dysfunctions in the female reproductive system and associated organs. This study proposes an investigation of the mammary gland (MG) in aged Mongolian gerbil (Meriones unguiculatus) mothers after their exposure to BPA in two windows of morphophysiological plasticity: pregnancy and lactation. A low dose (50 μg/kg) and a high dose (5000 μg/kg) of BPA were considered, and results showed few differences between them. As expected, we observed contrasts among control and BPA-exposed MG. The control groups presented a regressive phase with high apoptotic activity and elastic stroma. However, BPA damaged mammary tissue and provoked multifocal carcinoma development supported by an apparent epithelial-mesenchymal transition (EMT) and reactive stroma establishment. BPA remodeled stromal fibers deposition and enhanced the recruitment of tumor-associated cells, contributing to a tumoral microenvironment. Overexpression of TGF-β1 was induced by BPA in the epithelial compartment of exposed MG, and increased expression of metalloproteinases (MMP-2, MMP-3, MMP-9) was present in carcinoma cells. In conclusion, exposure of mothers to BPA during the gestational/lactational window of susceptibility leads to carcinogenic impacts with aging.


Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3047
Author(s):  
Jully Gogoi-Tiwari ◽  
Dorji Dorji ◽  
Harish Kumar Tiwari ◽  
Gayatri Shirolkar ◽  
Joshua W. Aleri ◽  
...  

Non-typeable (NT) Staphylococcus aureus strains are associated with chronic bovine mastitis. This study investigates the impact of biofilm formation by clinical NT S. aureus on cytokine production and mammary tissue damage by using a mouse mastitis model. Mice infected with two different NT S. aureus strains with strong and weak biofilm forming potential demonstrated identical clinical symptoms (moderate), minimal inflammatory infiltrates, and tissue damage (level 1 histopathological changes) in the mammary glands. However, the S. aureus load in the mammary glands of mice and the level of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, IL-17 and IFN-γ) in serum were significantly higher (p ≤ 0.05) in those infected with the strong biofilm forming NT S. aureus strain. The level of IL-6 in sera samples of these mice was extremely high (15,479.9 ± 532 Pg/mL. Furthermore, these mice died in 24h of post infection compared to 30 h in the weak biofilm forming NT S. aureus infected group. The study demonstrates no association between the strength of PIA (polysaccharide intercellular adhesion)-dependent biofilm production by clinical NT S. aureus and mammary gland pathology in a mouse mastitis model. However, the role of biofilm in the virulence of S. aureus advancing the time of mortality in mice warrants further investigation.


Author(s):  
Manobharathi Vengaimaran ◽  
Kalaiyarasi Dhamodharan ◽  
Mirunalini Sankaran

Background: Diosgenin, a steroidal saponin spotted as a primary ingredient in many traditional Chinese medicines, has sparked the attention of researchers owing to its multi-targeted cytotoxicity towards a multitude of cancers. Regrettably, its true potential was bounded by its impoverished physicochemical properties. In order to fully exploit its ability, we plan to fabricate diosgenin into nanoparticle by encapsulating with biodegradable polymer chitosan. Aim: The current research intends to uncover the therapeutic potency of diosgenin encapsulated chitosan nanoparticles (DG@CS-NP) on 7,12dimethylbenz(a)anthracene (DMBA) induced rat mammary carcinoma by optimizing biochemical and histopathological modifications via attenuating Aryl hydrocarbon receptor (AhR) - nuclear factor erythroid-derived 2-related factors (Nrf-2) signaling. Methodology: Breast cancer was induced with a single dose of DMBA (25 mg/kg b.wt). Orally supplied DG 10mg/kg b.wt. and DG@CS-NP 5 mg/kg b.wt to DMBA-induced tumor-bearing rats shortly after tumor onset. After the experimental period, biochemical and histopathological studies were performed using mammary tissue sections. Furthermore, architectural immunohistochemistry was used to reveal the expression of AhR and Nrf-2 in experimental rats. Additionally, diosgenin interactions with these proteins were also evidently confirmed by molecular docking analysis. Result: We noticed that there is an elevated level of lipid peroxidative marker, phase-I detoxification enzymes, total cholesterol (TC), phospholipids (PL), triglycerides (TG), and free fatty acids (FFA) with boosted AhR expressions as well as diminished levels of enzymatic and non-enzymatic antioxidants and Phase – II detoxification enzymes with downtrodden Nrf-2 expressions in the mammary tissues of DMBA-induced rats. On the other contrary, oral dosing of DG@CS-NP 5 mg/kg b.wt, dramatically reverted them to near-normal tiers. Interestingly, molecular docking analyses also corroborate these insights by highlighting diosgenin's significant interactions with AhR and Nrf-2 targets. Conclusion: As an outcome of our observations, we conclude that nano-encapsulation of diosgenin is a potent targeted therapeutic candidate posing a massive impact on breast cancer than plain diosgenin.


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