Berberine, an isoquinoline alkaloid purified from Chinese herbs, was verified to have antitumor effects. It has also been reported that berberine can enhance the anticancer effect of tamoxifen (TAM) in estrogen receptor (ER)-positive breast cancer cells; however, the involved underlying mechanism is still unclear. In the present study, the role of one variant of ER-α, ER-α36, in the TAM sensitizing effect of berberine was explored in TAM-resistant breast cancer cells. This study demonstrated that berberine potently sensitized TAM-resistant breast cancer cells, including TAM-resistant MCF7 and BT-474 cells, to TAM treatment. Additionally, this study showed that berberine could simultaneously suppress ER-α36 expression in TAM-resistant cells. However, when ER-α36 was knocked down in TAM-resistant cells, there was no significant TAM-sensitizing effect by berberine. Therefore, this study indicated that ER-α36 is involved in berberine’s TAM-sensitizing effect on ER-positive breast cancer cells, which provided supporting data for the application of berberine in cancer therapy as an adjuvant agent for TAM treatment.

Tamoxifen (TAM) is routinely used for the treatment of estrogen-positive breast carcinoma. Approximately 40% of patients with metastatic breast cancer will develop resistance to TAM. TAM therapeutic failure has been a major challenge in the treatment of TAM-resistant breast cancer cells. Therefore, finding a way to eliminate TAM resistance is very valuable. Curcumin is a polyphenol extracted from the rhizomes of Curcuma longa and has extensive biological and pharmacological effects on many cancers. The purpose of this study was to look into the effects of dendrosomal nano-curcumin (DNC) on cell growth and apoptosis, as well as the effects of DNC on the expression levels of long non-coding RNA CCAT2 in TAM-resistant MCF-7 cells (TAM-R). TAM-R cells were created, and CCAT2 expression was evaluated in TAM-R compared to TAM-sensitive MCF-7 cells (TAM-S). Forty eighth hours after TAM-R treatment with 20 μM of DNC, Q-RT-PCR, and flow cytometry cell cycle and Annexin V-PI assays were performed. P-value < 0.05 was defined as statistical significance. CCAT2 was significantly upregulated in TAM-R compared to TAM-S. DNC administration downregulated CCAT2 expression, and markedly suppressed cell cycle and induced apoptosis in TAM-R. Furthermore, DNC decreased the anti-apoptosis gene (BCL-2) and increased the apoptotic gene (BAX) expression levels respectively in TAM-R. DNC promoted cell cycle arrest and apoptosis, eventually by CCAT2 downregulation in TAM-R. However, the probable mechanisms of how DNC affects CCAT2 expression levels are unknown and need future studies.

Tamoxifen (TAM) is routinely used for the treatment of estrogen-positive breast carcinoma. Approximately 40% of patients with metastatic breast cancer will develop resistance to TAM. TAM therapeutic failure has been a major challenge in the treatment of TAM-resistant breast cancer cells. Therefore, finding a way to eliminate TAM resistance is very valuable. Curcumin is a polyphenol extracted from the rhizomes of Curcuma longa and has extensive biological and pharmacological effects on many cancers. The purpose of this study was to look into the effects of dendrosomal nano-curcumin (DNC) on cell growth and apoptosis, as well as the effects of DNC on the expression levels of long non-coding RNA CCAT2 in TAM-resistant MCF-7 cells (TAM-R). TAM-R cells were created, and CCAT2 expression was evaluated in TAM-R compared to TAM-sensitive MCF-7 cells (TAM-S). Forty eighth hours after TAM-R treatment with 20 μM of DNC, Q-RT-PCR, and flow cytometry cell cycle and Annexin V-PI assays were performed. P-value < 0.05 was defined as statistical significance. CCAT2 was significantly upregulated in TAM-R compared to TAM-S. DNC administration downregulated CCAT2 expression, and markedly suppressed cell cycle and induced apoptosis in TAM-R. Furthermore, DNC decreased the anti-apoptosis gene (BCL-2) and increased the apoptotic gene (BAX) expression levels respectively in TAM-R. DNC promoted cell cycle arrest and apoptosis, eventually by CCAT2 downregulation in TAM-R. However, the probable mechanisms of how DNC affects CCAT2 expression levels are unknown and need future studies.

Tamoxifen (TAM) is an important drug for treatment of breast cancer. It is most effective against estrogen receptor-positive and negative breast cancer. Protective adjuvant is another applied of TAM for women at risk of development of breast cancer. Anti-cancer activity of TAM can take various pathways of action. Antagonistic with estrogen receptor and oxidation reaction are the most proposed mechanism of action of TAM in cancer cells. Recently, many studies focused on the potential antimicrobial action of TAM. Fungi are demonstrated to affect by TAM through various mechanism of action. Yeasts, especially Candida albicans</em>, are the most common type of fungi used to test the antifungal action of TAM. Inhibitory action on some components of the calcium-calcineurin pathway in fungal cells is most acceptable mechanism of TAM action. TAM can also play a synergistic role to increase the antifungal activity of other standard agents. This review will discuss the most recent information about antifungal action of TAM.

Breast cancer (BC) is the most epidemic malignancy of women worldwide that leads to cause of morbidity and mortality. Tamoxifen (TAM) is the common therapy used in the BC treatment. Monoamine oxidases are enzymes linked to the progression of many types of carcinomas through its consideration on the production of reactive oxygen species. This study aimed to clarify the correlations between MAO isoforms (MAOs), atherogenic index, TAM, and their roles in the BC progression. 60 newly diagnosed and 60 TAM treated women with BC, as well as 50 healthy volunteers were included in this study. Parameters including MAOs activities, lipid profile, malondialdehyde, and total protein were determined before and after treatment with TAM. The activities of total MAO, MAO-A, MAO-B, and semi-carbazide-sensitive amine oxidase (SSAO) were significantly (P<0.0001) decreased in newly diagnosed and TAM-treated women compared with healthy individual. However, the activities of all tested enzymes were elevated significantly (P<0.0001) in TAM-treated women compared with the newly diagnosed women. The strong positive correlations were found among MAOs in response to TAM treatment. Receiver operating characteristic showed a higher sensitivity and specificity for MAOs in discrimination between newly diagnosed and TAM-treated women. Atherogenic index was significantly increased (P<0.0001) in newly diagnosed and in TAM-treated women compared with control. The findings of this study indicated that BC patients are more vulnerable to cardiovascular diseases, independent of TAM and MAOs effect. Based on the forgoing, MAOs can be used as a diagnostic marker for BC progression.

Histone deacetylation of tumor suppressor genes such as estrogen receptor alpha (ERα) can induce cancer, which is reversible by epi-drugs such as valproic acid (VPA). The previous result indicated that tamoxifen (TAM) induced apoptosis in hepatocellular carcinoma (HCC). This study was designed to assess the apoptotic and antiproliferative effects of VPA and TAM and also the effect of VPA on ERα gene expression in HCC.
Material and The cells were treated with various doses of VPA and TAM and the MTT assay, Real-Time RT-PCR, and flow cytometry assay were done to determine viability, ERα gene expression, and apoptosis.
Both agents inhibited viability and induced apoptosis. ERα gene expression was increased by VPA, which in turn increased the apoptotic effect of TAM. The half-maximum inhibitory concentration (IC50) value for VPA and TAM was 5 and 20 μM respectively. VPA inhibited cell growth by 88 % to 38 % at 24 h (P VPA and TAM can significantly inhibit viability and induce apoptosis and also VPA play a significant role in ERα reactivation.

Tamoxifen (TAM) is a selective estrogen receptor modulator used in the treatment of breast cancer, women’s infertility and some other endocrine diseases. TAM is a generic medication that is prescribed relatively a lot. Due to the impact of this medication and its side effects, screening TAM level in biological samples and in pharmaceutical formulations are of great importance. Various analytical techniques are developed for the detection or monitoring TAM levels in different matrices. Since TAM chemical structure is able to undergo electrochemical oxidation, electrochemical techniques due to their remarkable features are also considered as analytical methods. Here, electroanalytical measurements of TAM will be reviewed.

Colloidal drug delivery system, solid lipid nanoparticles (SLNs), helps to increase the solubility of the drug and its oral bioavailability. Tamoxifen (TAM) as a nonsteroidalantiestrogen drug was formulated in SLN and an in vitro study was conducted to determine the cytotoxicity effect of TAM-loaded SLNs on human breast cancer cell lines MCF-7 (estrogen receptor-positive) and MDA-MB231 (estrogen receptor-negative) cells. The cytotoxicity was measured by (3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assay). The results showed that tamoxifen-loaded SLNs has an equally efficient cytotoxic activity against MCF-7 and MDA-MB231 cells, compared with free tamoxifen, and the half maximal inhibitory concentration (IC50) of TAM-loaded SLNs was generally lower than that of free TAM. This finding indicates that tamoxifen’s cytotoxicity may result from improved drug internalization through encapsulation into the SLN matrix and endocytosis. Therefore, when TAM is incorporated into the SLN carrier system, its antitumoral activity is still preserved, suggesting that SLN is a good carrier for the drug insoluble in water.

Current research had successfully encapsulated magnetic nanoparticles (MNP) with selective estrogen receptor drug tamoxifen citrate (TAM) using Poly (d,l-lactice-co-glycolide acid) (PLGA 75:25) via oil in water emulsion technique. TAM is a good example of a drug that is difficult to dissolve. TAM is currently approved for the treatment of hormone-sensitive and early-stage breast cancer as an adjuvant endocrine therapy. The majority of the prescription medicine in today market is made up of poorly soluble, bioavailable, and quickly metabolized and eliminated drug which is a continuously challenges up to these days. Therefore, it is imperative to overcome this disadvantages by encapsulating TAM inside PLGA together with MNP for improved drug delivery. The MNP coated with oleic acid (OA) was synthesized using co-precipitation method and it is known as OAMNP. The fabricated nanohybrid is known as TAM-PLGA-OAMNP where the TAM was encapsulated together with OAMNP within PLGA. XRD results showed that OAMNP is Fe3O4. FTIR spectra revealed that the TAM was successfully encased into the PLGA structure. TAM-PLGA-OAMNP average size is about 131 ± 28 nm as shown in TEM results. The nanohybrid nanoparticles showed the absence of hysteresis loop indicative of superparamagnetic properties.

Consumption of a high-fat diet (HFD) is associated with an increased incidence of inflammatory diseases and metabolic disorders. Also, these disorders will increase in women with aging and menopause, which is probably due to the reduced role of estradiol (E2). Selective estrogen modulators including tamoxifen (TAM), which acts through estrogen receptors, have important metabolic effects. This study aimed to determine whether TAM and E2 have protective effects on inflammation caused by HFD in young and aged mice. Four-month-old (Sham and ovariectomized [OVX]) and 20-month-old female C57BL/6J mice were used in this study. After feeding them with HFD for 12 weeks, they were divided into nine groups consisting of Sham + Oil, Sham +TAM, Sham + E2, OVX + Oil, OVX +TAM, OVX + E2, Aged + Oil, Aged +TAM, and Aged + E2. TAM and E2 were injected subcutaneously every four days for four weeks. At the end of the experiments, the mice’s blood was sampled. The serum cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) were also determined using ELISA kits. The results revealed that HFD increased inflammation by reducing IL-10 and increasing TNF-a/IL-10 and IL-6/IL-10 ratio in young and aged mice, and TAM and E2 therapy resulted in a significant decrease in TNF-α and IL-6, and an increase in IL-10 in young and aged mice. In conclusion, the results of this study indicated that TAM, in addition to being used as an anticancer drug, can reduce HFD-induced inflammation in both young and aged mice. Therefore, probably it is a good candidate to substitute E2.