Category: SDGs-2024

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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SDGs, SDGs-2024

Formulation development of thermoresponsive quercetin nanoemulgels and in vitro investigation of their inhibitory activity on vascular endothelial growth factor-A inducing neovascularization from the retinal pigment epithelial cells

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

Formulation development of thermoresponsive quercetin nanoemulgels and in vitro investigation of their inhibitory activity on vascular endothelial growth factor-A inducing neovascularization from the retinal pigment epithelial cells

Quercetin is a natural plant that can help prevent the growth of new blood vessels, which is a common problem in certain eye diseases and cancers. This effect is due to quercetin’s ability to block the activity of a protein called VEGF-A, which plays a key role in promoting blood vessel growth. However, quercetin doesn’t dissolve well in water, making it difficult to deliver effectively to the eye. To address this, researchers developed a new, temperature-sensitive gel formulation, called T-QNE-G, that can carry quercetin and be injected into the eye.

This gel stays liquid at room temperature, making it easy to inject, and then turns into a gel at body temperature, allowing it to stay in place within the eye. The results showed the optimized gel (S–2F127–1F68) was able to reduce the movement and formation of blood vessels in human eye cells and reduce VEGF-A activity. This suggests that S–2F127–1F68 could be a promising treatment for eye diseases that involve abnormal blood vessel growth. Further testing in animal models will help determine its effectiveness and safety for future treatments.

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