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Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer.

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Endoplasmic reticulum (ER) stress is an intriguing target with significant clinical importance in chemotherapy. Interference with ER functions can lead to the accumulation of unfolded proteins, as detected by transmembrane sensors that instigate the unfolded protein response (UPR). Therefore,

Test of catechol, tannic acid, Bidens pilosa, croton oil, and phorbol for cocarcinogenesis of esophageal tumors induced in rats by methyl-n-amylnitrosamine.

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Catechol (CAS: 120-80-9), given in drinking water to rats, was the most effective of 5 phenols in enhancing [3H]thymidine incorporation [( 3H]dThd-l) into esophageal DNA. To test for esophageal cocarcinogenesis, groups of 30 male MRC-Wistar rats received 3 weekly ip injections of 25 mg

Tannic acid ameliorates doxorubicin-induced cardiotoxicity and potentiates its anti-cancer activity: potential role of tannins in cancer chemotherapy.

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Doxorubicin, an anthracycline antibiotic, is widely used in the treatment of various solid tumors including breast cancer. However, its use is limited due to a variety of toxicities including cardiotoxicity. The present study aimed to evaluate the effect of tannic acid, a PARG/PARP inhibitor and an

Combination of quercetin and tannic acid in inhibiting 26S proteasome affects S5a and 20S expression, and accumulation of ubiquitin resulted in apoptosis in cancer chemoprevention.

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To look for oral proteasome inhibitors, daily injested food is the best source for cancer chemoprevention. A combination of active components from vegetables, coffee, tea, and fruit could be more efficient to inhibit 26S proteasome activities for preventing cancer diseases. Tannic acid and quercetin

Tannic Acid preferentially targets estrogen receptor-positive breast cancer.

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Research efforts investigating the potential of natural compounds in the fight against cancer are growing. Tannic acid (TA) belongs to the class of hydrolysable tannins and is found in numerous plants and foods. TA is a potent collagen cross-linking agent; the purpose of this study was to generate

Inhibition of tumor promoter-induced ornithine decarboxylase activity by tannic acid and other polyphenols in mouse epidermis in vivo.

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Naturally occurring plant phenols with antimutagenic and anticarcinogenic activities were tested for their abilities to inhibit the ornithine decarboxylase (ODC) response linked to skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Topical applications of tannic acid (TA) inhibit

HER2+ breast cancer cells undergo apoptosis upon exposure to tannic acid released from remodeled cross-linked collagen type I.

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Tannic acid (TA) is a naturally occurring polyphenol that cross-links collagen type I and possesses anticancer potential. In previous studies, we demonstrated the increased sensitivity of estrogen receptor-positive (ER+ ) breast cancer cells to TA as opposed to triple negative breast cancer cells

Tannic Acid-Lung Fluid Assemblies Promote Interaction and Delivery of Drugs to Lung Cancer Cells.

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Lung cancer (LC) is one of the leading causes of death in both men and women in the United States. Tannic acid (TA), a water-soluble polyphenol, exhibits a wide range of biological activities. TA has received much attention as a promising compound in the biomaterial and drug delivery fields. Lung

Tannic acid cross-linked collagen scaffolds and their anti-cancer potential in a tissue engineered breast implant.

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Tannic acid (TA) is a hydrolysable plant tannin, and it has been determined that TA functions as a collagen cross-linking agent through hydrogen-bonding mechanisms and hydrophobic effects. Since TA may have anti-tumor properties, it may be a viable cross-linking agent for collagen-based breast

Remodeling of tannic acid crosslinked collagen type I induces apoptosis in ER+ breast cancer cells.

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BACKGROUND The naturally-occurring phytochemical tannic acid (TA) has anticancer properties. We have demonstrated that estrogen receptor-positive (ER+) breast cancer cells are more sensitive to effects of TA than triple-negative breast cancer cells and normal breast epithelial cells. In the present

Tannic acid synergistically enhances the anticancer efficacy of cisplatin on liver cancer cells through mitochondria‑mediated apoptosis.

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Cisplatin (cis‑dichlorodiamine platinum, CDDP) is a potent antitumor agent. However, its clinical application is limited by its side effects and the development of drug resistance. Tannic acid (TA) has previously been reported to suppress tumor growth in different types of cancer. The present study

Tannic Acid Inhibits Non-small Cell Lung Cancer (NSCLC) Stemness by Inducing G ₀/G ₁ Cell Cycle Arrest and Intrinsic Apoptosis

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Background/aim: Non-small cell lung cancer (NSCLC) is one among the most common cancers worldwide. Recently, dietary phytochemicals have been reported as an attractive approach to improve the symptoms of NSCLC patients. Tannic acid is a

Tannic acid potently inhibits tumor cell proteasome activity, increases p27 and Bax expression, and induces G1 arrest and apoptosis.

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Animal studies have demonstrated that a dietary polyphenol known as tannic acid (TA) exhibits anticarcinogenic activity in chemically induced cancers, although the involved molecular target remains unknown. In addition, proteasome inhibitors have been shown to suppress human tumor growth in nude

Tannic acid mitigates the DMBA/croton oil-induced skin cancer progression in mice.

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Skin cancer is the most common malignancy in the world and also one of the major causes of death worldwide. The toxic environmental pollutant 7,12-dimethylbenz[a]anthracene (DMBA) is a skin-specific carcinogen. Tannic acid (TA) is reported to be effective against various types of chemical-induced

Pectin-Tannic Acid Nano-Complexes Promote the Delivery and Bioactivity of Drugs in Pancreatic Cancer Cells.

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Pancreatic cancer (PanCa) is a lethal disease. Conventional chemotherapies for PanCa offer severe systemic toxicities. Thus, the development of a successful nanomedicine-based therapeutic regimen with augmented therapeutic efficacy is highly sought. Naturally occurring pectin and modified

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tannic acid/cancro

Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer.

Test of catechol, tannic acid, Bidens pilosa, croton oil, and phorbol for cocarcinogenesis of esophageal tumors induced in rats by methyl-n-amylnitrosamine.

Tannic acid ameliorates doxorubicin-induced cardiotoxicity and potentiates its anti-cancer activity: potential role of tannins in cancer chemotherapy.

Combination of quercetin and tannic acid in inhibiting 26S proteasome affects S5a and 20S expression, and accumulation of ubiquitin resulted in apoptosis in cancer chemoprevention.

Tannic Acid preferentially targets estrogen receptor-positive breast cancer.

Inhibition of tumor promoter-induced ornithine decarboxylase activity by tannic acid and other polyphenols in mouse epidermis in vivo.

HER2+ breast cancer cells undergo apoptosis upon exposure to tannic acid released from remodeled cross-linked collagen type I.

Tannic Acid-Lung Fluid Assemblies Promote Interaction and Delivery of Drugs to Lung Cancer Cells.

Tannic acid cross-linked collagen scaffolds and their anti-cancer potential in a tissue engineered breast implant.

Remodeling of tannic acid crosslinked collagen type I induces apoptosis in ER+ breast cancer cells.

Tannic acid synergistically enhances the anticancer efficacy of cisplatin on liver cancer cells through mitochondria‑mediated apoptosis.

Tannic Acid Inhibits Non-small Cell Lung Cancer (NSCLC) Stemness by Inducing G 0/G 1 Cell Cycle Arrest and Intrinsic Apoptosis

Tannic acid potently inhibits tumor cell proteasome activity, increases p27 and Bax expression, and induces G1 arrest and apoptosis.

Tannic acid mitigates the DMBA/croton oil-induced skin cancer progression in mice.

Pectin-Tannic Acid Nano-Complexes Promote the Delivery and Bioactivity of Drugs in Pancreatic Cancer Cells.

O mais completo banco de dados de ervas medicinais apoiado pela ciência

Tannic Acid Inhibits Non-small Cell Lung Cancer (NSCLC) Stemness by Inducing G ₀/G ₁ Cell Cycle Arrest and Intrinsic Apoptosis