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The present study aimed to investigate whether rhamnetin induced apoptosis in human breast cancer cells and the underlying molecular mechanism of this anti cancer effect. The treatment of MCF-7 cells with rhamnetin was able to significantly inhibit cell proliferation and induce caspase-3/9 activity in a dose- and time-dependent manner, compared with untreated cells. In addition, treatment with rhamnetin was able to significantly promote the expression of p53 protein and microRNA (miR-)34a compared with untreated cells. The treatment with rhamnetin also suppressed the expression of Notch1 protein in MCF-7 cells compared with untreated cells. Subsequently, miR-24a expression was promoted in rhamnetin-treated MCF-7 cells using a miR-34a plasmid. The overexpression of miR-34a was able to significantly inhibit cell viability and induce caspase-3/9 activity in MCF-7 cells following treatment with rhamnetin. Furthermore, the overexpression of miR-34a was able to significantly promote the expression of p53 protein and miR-34a, and suppress the expression of Notch1 protein in rhamnetin-treated MCF-7 cells. Therefore, the results of the present study demonstrated that rhamnetin induced apoptosis in human breast cancer cells via the miR-34a/Notch-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Capecitabine monotherapy is usually used for advanced breast cancer (ABC) resistant to anthracycline and taxane, but there are still many other options too. Our meta-analysis assessed whether capecitabine monotherapy was superior or noninferior to the other regimens in ABC pretreated with anthracycline and taxane.Materials and Methods: PubMed databases and abstracts from the proceedings of American Society of Clinical Oncology and San Antonio Breast Cancer Symposium were searched for randomized controlled trials that compared capecitabine monotherapy with other regimens for ABC progression after anthracycline- and taxane-treatment. Hazard ratios (HRs) were used for progression-free survival (PFS) and overall survival (OS). Risk ratios (RRs) were used for overall response rate (ORR) and Grade 3-4 drug-related adverse events. All statistical analyses were conducted with RevMan 5.3 software, and statistical significance was defined as P < 0.05.Results: In total, 4671 patients from eight trials were included. Target therapy as treatment group was involved in four trials, and the other four trials were merely chemotherapy in treatment group. Our study indicated that capecitabine monotherapy was not superior but also noninferior to the other regimens in ORR (RR = 1.32-95% confidence interval [CI] 0.98-1.77, P = 0.07), PFS (HR = 1.03, 95% CI 0.85-1.25, P = 0.76), and OS (HR = 0.96, 95% CI 0.88-1.05, P = 0.40). Subgroup analysis showed that both the other chemotherapy regimens and target drugs failed to improve efficacy compared with capecitabine monotherapy, and target drugs could shorten PFS (HR = 1.22, 95% CI 1.06-1.39, P = 0.004). Incidences of Grade 3-4 hematology toxicity in other regimens group significantly increased compared with capecitabine monotherapy.Conclusions: Our meta-analysis demonstrated that capecitabine monotherapy could be the first choice for ABC pretreated with anthracycline and taxane due to its efficacy and low toxicity. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effects of NF-κB activation on the proliferation and apoptosis throughTLR4/MyD88 signaling pathway in human nasopharyngeal carcinoma (NPC) 5-8F cell lines., Method: TLR4 induced by LPS is inhibited by PE anti-human. Real-Time Quantitative PCR and Western blot were employed to evaluate the efficacy of mRNA level and protein expression. The growth inhibition rate of 5-8F by Celecoxib was evaluated with MTT method. The cell cycle and apoptosis were measured with flow cytometric method (FCM)., Result: By using the specific inhibitor, the protein and gene expression of NF-κB and MyD88 were both significantly lower than the control group (P<. 05). Meanwhile, the down-rugulation of NF-κB could inhibit proliferation of NPC 5-8F cells and promote their apoptosis (P<0. 05)., Conclusion: By inhibiting TLR4 / MyD88 signaling pathway, the expression of NF-κB in NPC 5-8F cells could decrease, then the cell proliferation was inhibited and cell apoptosis was induced. The results showed that TLR4 / MyD88 / NF-κB induced by LPS is an important pathway in the genesis and development of NPC. This study provides evidence for targeting research of NPC.

Objective: To compare the efficacy of lapatinib or lapatinib plus trastuzumab versus trastuzumab in the neoadjuvant therapy of human epidermal growth factor receptor 2 (HER-2) positive breast cancer., Methods: MEDLINE database, American Society of Clinical Oncology (ASCO), San Antonio Breast Cancer Symposium (SABCS), European Society for Medical Oncology (ESMO) proceedings and China Biomedical Database were searched for literatures of trastuzumab or lapatinib in neoadjuvant therapy for breast cancer. There was no limit of language or time. A meta-analysis was performed for retrieved literatures meeting the inclusion criteria., Results: A total of 1 794 breast cancer patients from 5 clinical trials were included. And the regimens were lapatinib plus neoadjuvant chemotherapy (n = 719), trastuzumab plus neoadjuvant chemotherapy (n = 714) and both drugs plus neoadjuvant chemotherapy (n = 361). The rate of pathological complete remission (pCR) was lower in lapatinib group than that in trastuzumab group (28.2% vs 35.4%). And the difference was statistically significant (P = 0.004). The pCR rate was significantly higher in lapatinib plus trastuzumab therapy group than that in trastuzumab group (53.2% vs 38.1%, P < 0.001)., Conclusions: Lapatinib can not replace trastuzumab as a first-choice agent in neoadjuvant therapy of HER-2 positive breast cancer. Lapatinib plus trastuzumab achieves better pCR than trastuzumab so that it and may become a first-choice of neoadjuvant therapy for HER-2 positive breast cancer regardless of economic affordability for patients.