Curcumin induces autophagic cell death in human thyroid cancer cells.
In the present study, curcumin significantly inhibited the growth of thyroid cancer cells.
Thyroid Cancer · LIVING RESEARCH LIBRARY
Ongoing Research for Thyroid Cancer Using Advanced Alternative Medicine
Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
Every entry includes the original study title, year, concise finding and a direct PubMed link.
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Research organized by substance and finding
Browse 12 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
Open study on PubMed →
Curcumin Induces Ferroptosis in Follicular Thyroid Cancer by Upregulating HO-1 Expression.
Tumorigenesis is significantly inhibited by curcumin.
Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691.
We observed that curcumin treatment decreased B-CPAP cell proliferation and promoted apoptosis.
The curcumin analogue PAC has potent anti-anaplastic thyroid cancer effects.
This anti-EMT effect was confirmed by showing PAC-dependent inhibition of the proliferation and migration abilities of ATC cells.
Ginsenoside Rh2 inhibits thyroid cancer cell migration and proliferation via activation of miR-524-5p.
Ginsenoside Rh2 is known as an anticancer molecule; however, its function in thyroid cancer cells has not been reported.
Gut microbiota and metabolite profiles in thyroid cancer lymph node metastasis: a multi-omics analysis.
Our study underscores the potential influence of gut microbiota and metabolites on the advancement and metastasis of thyroid cancer progression.
Tumor microbiome diversity influences papillary thyroid cancer invasion.
Here, using 16S RNA sequences, we analyzed the PTC intratumor microbiome and its role in tumor progression.
Targeting S1PR1 in Thyroid Cancer: Functional Characterization and Proteasome-Mediated Suppression by Quercetin.
Furthermore, we screened several anticancer compounds to determine their effects on S1PR1 expression levels in thyroid cancer cells and found that quercetin significantly reduced S1PR1 protein levels in these cells.
Mechanism of cancer-associated fibroblast-driven thyroid cancer dedifferentiation via the ZFP57-PKM2 axis-mediated lactate secretion and therapeutic intervention with resveratrol.
Resveratrol (Res), a natural compound, has shown anticancer potential by promoting redifferentiation and apoptosis while inhibiting oncogenic signaling, suggesting utility in countering PTC dedifferentiation.
Vitamin C induces ferroptosis in anaplastic thyroid cancer cells by ferritinophagy activation.
The present study demonstrated that vitamin C could significantly inhibit ATC cells growth through ferroptosis activation, evidenced by the GPX4 inactivation, ROS accumulation and iron-dependent lipid peroxidation.
Association of Vitamin D Pathway Genetic Variation and Thyroid Cancer.
Genetic variants close to genes that encode crucial enzymes for the synthesis (DHCR7 rs12785878), metabolism (CYP2R1 rs2060793) and degradation (CYP24A1 rs6013897) of vitamin D have been associated with serum levels of vitamin D.
Evaluation of Vitamin D3 levels and dietary management in patients with papillary thyroid cancer.
After 12 weeks of VitD3 supplementation (insufficient patients received1000IJ/day, deficient patients 2000IJ/day, severe deficient patient 5000IJ/day) along with the lifestyle and dietary management, the response was evaluated according to the personal characteristics, levels of VitD, free thyroxine (FT4), freetriiodothyronine (FT3) hormones and thyroglobulin (TG).
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