Category: SDGs-2024

SDGs, SDGs-2024

Male reproductive phenotype alterations in heterozygous β-globin gene knockout thalassemia (BKO) mice as a model for β-thalassemia patients

Goals 3
Ensure healthy lives and promote well-being for all at all ages

Male reproductive phenotype alterations in heterozygous β-globin gene knockout thalassemia (BKO) mice as a model for β-thalassemia patients

Beta-thalassemia mice and wild type mice were loaded with iron dextran to mimic iron overload, while unloaded mice served as control groups to study its effect on the male reproductive system. Iron-loaded mice showed significantly increased blood and testis iron levels but exhibited reduced testosterone, sperm count, and the number of sperm with normal morphology. Iron accumulated in the anterior pituitary and testicular interstitium but did not cause significant tissue changes. Therefore, iron-loaded thalassemia mice exhibit reproductive dysfunction and abnormal sperm, which could be a concern and should be further investigated in patients.

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SDGs, SDGs-2024

A Potential Combination of Targeting HSP90 and mTOR in Breast Cancer Cell Growth, Migration, and Invasion Through Inhibiting AKT Phosphorylation and F-actin Organization

Goals 3
Ensure healthy lives and promote well-being for all at all ages

A Potential Combination of Targeting HSP90 and mTOR in Breast Cancer Cell Growth, Migration, and Invasion Through Inhibiting AKT Phosphorylation and F-actin Organization

Breast cancer is the most common cancer among women worldwide and has a high death rate, mainly due to metastasis. Unfortunately, no effective treatment is available for metastatic breast cancer. The potential of combining HSP90 and mTOR inhibitors to treat breast cancer cell growth, migration, and invasion was explored in this study. Gene expression profiles were examined using Gene Expression Profiling Interactive Analysis (GEPIA).

Protein expression and localization were studied using Western blot analysis and fluorescence staining. Cell proliferation, migration, and invasion were assessed using MTT, wound healing, and transwell invasion assays. It was found that HSP90 expression was significantly higher in breast invasive carcinoma compared to other tumor types, and this high expression was linked to mTOR levels. Cell proliferation was significantly inhibited by treatment with 17-AAG (an HSP90 inhibitor) and Torkinib (an mTORC1/2 inhibitor). AKT signaling was reduced, F-actin intensity was decreased, and YAP levels were lowered by the combination treatment, disrupting its nuclear localization.

In conclusion, breast cancer cell growth and progression can be suppressed by targeting HSP90 and mTOR, which interferes with AKT signaling and inhibits F-actin polymerization. This combination treatment shows promise as a therapeutic strategy for breast cancer, potentially reducing the adverse effects of single treatments.

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SDGs, SDGs-2024

17-AAG Induces Endoplasmic Reticulum Stress-mediated Apoptosis in Breast Cancer Cells, Possibly Through PERK/eIF2α Up-regulation

Goals 3
Ensure healthy lives and promote well-being for all at all ages

17-AAG Induces Endoplasmic Reticulum Stress-mediated Apoptosis in Breast Cancer Cells, Possibly Through PERK/eIF2α Up-regulation

This study explored how 17-AAG, a drug that blocks the heat shock protein HSP90, might work to kill breast cancer cells. Using a pharmacology network and gene analysis, researchers identified that HSP90 could be a key connection between 17-AAG and genes linked to breast cancer. Lab tests showed that 17-AAG slowed down cell growth and triggered cell death in breast cancer cells. The drug also raised cellular oxidant levels and increased stress-related proteins, PERK and eIF2α. Further tests showed that this protein stress led to DNA damage, suggesting a breakdown in cell function. The study highlights HSP90 as a potential treatment target for breast cancer, with 17-AAG showing promise as a therapy that disrupts cellular stress pathways to induce cancer cell death.

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SDGs, SDGs-2024

Skin anti-aging and wound healing effects of a passion fruit seed extract rich in piceatannol

Goals 3
Ensure healthy lives and promote well-being for all at all ages

Skin anti-aging and wound healing effects of a passion fruit seed extract rich in piceatannol

UVB radiation accelerates skin aging by increasing cellular oxidants, leading to senescence and excess production of MMP-1, which causes wrinkles and delays wound healing. Passion fruit seeds (PFS) are rich in piceatannol (PCT), known for its antioxidant and anti-aging properties.

This study examined the effects of PFS extract on UVB-exposed skin cells (HaCaT). The extract, rich in PCT, reduced cellular oxidants, decreased senescence, and lowered MMP-1 production at both protein and mRNA levels.

It also promoted wound healing by enhancing cell migration and increasing EGFR mRNA expression. Additionally, SIRT1 production, associated with cellular rejuvenation, was boosted.

In conclusion, PFS extract shows promise for skincare and wound healing by reducing skin aging effects and supporting tissue repair.

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SDGs, SDGs-2024

Role of Oxidative Stress-Dependent C/EBPβ Expression on CAF Transformation Inducing HCT116 Colorectal Cancer Cell Progression; Migration and Invasion

Goals 3
Ensure healthy lives and promote well-being for all at all ages

Role of Oxidative Stress-Dependent C/EBPβ Expression on CAF Transformation Inducing HCT116 Colorectal Cancer Cell Progression; Migration and Invasion

Previous studies show that cancer-associated fibroblasts (CAFs) help cancer grow and spread, affecting patient outcomes. To develop better treatments, it’s crucial to understand how fibroblasts (FBs) turn into CAFs. The tumor microenvironment (TME) is like a chronic wound with ongoing inflammation, so FB activation in CAFs might be similar to FB activation in chronic inflammation. We suspected that the C/EBPβ protein, which increases in FBs during chronic inflammation, might also play a role in FB activation into CAFs.

This study aimed to explore the role of C/EBPβ in oxidative stress-related CAF transformation and its impact on colorectal cancer (CRC) progression. We used conditioned media (CM) from HCT116 CRC cells to activate CCD-18Co colon fibroblasts and assessed their ability to support HCT116 growth and spread using various assays. We also studied changes in the cytokine profile and oxidative stress of activated FBs.

Results showed that CM from HCT116 cells induced oxidative stress, changes in cytokine profile, CAF markers, and C/EBPβ expression in activated FBs. When oxidative stress was reduced, FAP and C/EBPβ expression decreased, and the FBs’ ability to support cancer progression was impaired. High C/EBPβ expression was linked to poor prognosis in CRC patients.

In conclusion, C/EBPβ plays a role in CAF transformation related to oxidative stress and could be a target for improving treatment outcomes in aggressive CRC.

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