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The effect of silencing the Tip60 gene on the response to radiotherapy in breast cancer cells
In this study, for the first time, the role of the silenced and active Tip60 gene in response to radiotherapy in MDA-MB-231 and MCF-7 cells was investigated. For this purpose, the Tip60 gene was silenced by applying siRNA to the cell lines and UV was applied. In the study, cytotoxicity and DNA breaks were measured by MTT and COMET methods, and mRNA and protein expression values were measured by PCR and Raman spectrophotometer in silenced, unsilenced, UV-treated, and non-UV-treated cell lines. According to the results of the study, increased DNA damage was observed in MCF-7 cell lines in which the Tip60 gene was silenced, a...
Source: Breast - April 17, 2023 Category: Cancer & Oncology Authors: Ece Miser-Saliho ğlu Bensu Karahalil Meri ç Arda Eşmakaya U ğur Tamer Sevgi Yardim-Akaydin Source Type: research

Icariin Alleviates Wear Particle-Induced Periprosthetic Osteolysis via Down-Regulation of the Estrogen Receptor α-mediated NF-κB Signaling Pathway in Macrophages
In conclusion, icariin attenuates wear particle-induced inflammation and osteolysis via down-regulation of the ERα-mediated NF-κB signaling pathway in macrophages. The potential application of icariin as a non-hormonal therapy for wear particle-induced periprosthetic osteolysis is worthy of further investigation.
Source: Frontiers in Pharmacology - November 3, 2021 Category: Drugs & Pharmacology Source Type: research

Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin
Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin. Introduction Endometrial cancer (EC) comprises the most common malignancy involving the female genital tract and the fourth most common malignancy in women after breast, lung, and colorectal cancers (1). In 2012, approximately 320,000 new cases of EC were diagnosed worldwide and the incidence is increasing (2). Currently, endometrial carcinogenesis is thought to be a multi-step process involving the coordinated interaction of hormonal regulation, gene mutation, ad...
Source: Frontiers in Oncology - April 10, 2019 Category: Cancer & Oncology Source Type: research

Abstract 2312: Identifying novel cancer stem cell target for triple-negative breast cancer
The objective of this study was to investigate the role of HN1L in regulating BCSC and metastasis in TNBC, and to determine the mechanism of action of HN1L in BCSC. Knocking down HN1L by shRNA in SUM159 and MDAMB231 cell lines significantly decreased mammosphere forming efficiency (MSFE) and CD44+/CD24low/- population. To assess the contribution of HN1L to BCSC and tumor growth, a patient derived human-cancer-in-mouse xenograft model and two cancer cell line xenograft models were employed. To ensure targeted delivery, siRNA was packaged into DOPC liposomes and delivered into mice via intraperitoneal injection. Results show...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Liu, Y., Choi, D. S., Grandos-Principal, S., Qian, W., Burey, L., Wong, H., Rodriguez-Aguayo, C., Sood, A., Li, Z., Wong, S., Weiss, H., Dave, B., Landis, M., Chang, J. C. Tags: Tumor Biology Source Type: research

Abstract P3-05-11: Glutamine metabolism promotes survival through the unfolded protein response in endocrine resistant breast cancer
About 70% of all breast cancers are estrogen receptor alpha positive (ER+). Anti-hormone therapy such as antiestrogens (e.g.,Tamoxifen; TAM) are often used to treat ER+ breast cancer but breast cancer cells can develop resistance to these drugs (endocrine resistance). Unfortunately, ∼50% percent of all antiestrogen treated tumors eventually develop endocrine resistance, and therefore, there is an urgent need to find ways to treat this incurable disease. Endocrine resistant cells survive antiestrogen treatment by initiating a pro-survival pathway mediated by an evolutionary conserved process call the unfolded protein resp...
Source: Cancer Research - April 30, 2015 Category: Cancer & Oncology Authors: Shajahan-Haq, A. N., Demo, S., Clarke, R. Tags: Poster Session Abstracts Source Type: research

Abstract B50: MEK inhibitors mount a two-pronged attack to kill estrogen receptor positive (ER+) breast cancer cells undergoing hormonal therapy: Attenuated autophagy and induction of apoptosis
In this study, we hypothesized that the requirement of MEK1/MAPK1/2 for pro-survival autophagy is due, in part, to its role in blocking the intracellular accumulation of dephosphorylated BimEL. To test this hypothesis, we modulated the expression of dephosphorylated BimEL with either a BimEL cDNA expression vector, siRNA targeting of BimEL, or MEK1 blockade with the small molecule inhibitor U0126 and determined the levels of the autophagic flux in ER+ breast cancer cells undergoing antiestrogen treatment. The determination of autophagic flux was made by comparing the levels of two proteins involved in autophagy -the LC3 /A...
Source: Molecular Cancer Research - February 5, 2015 Category: Cancer & Oncology Authors: Takhar, S., Manning, M., Eason, A., Dix, M., Periyasamy-Thandavan, S., Padi, R., Bieberich, E., Hill, W., Browning, D., Ganapathy, V., Thangaraju, M., Schoenlein, P. V. Tags: RAS Targeting: Poster Presentations - Proffered Abstracts Source Type: research

17-beta estradiol inhibits oxidative stress-induced accumulation of AIF into nucleolus and PARP1-dependent cell death via estrogen receptor alpha.
Abstract Oxidative stress-induced DNA damage results in over-activation of poly(ADP-ribose) polymerase 1 (PARP1), leading to parthanatos, a newly discovered cell elimination pathway. Inhibition of PARP1-dependent cell death has shown to improve the outcome of diseases, including stroke, heart ischemia, and neurodegenerative diseases. In the present study we aimed to detect whether estrogen plays a protective role in inhibiting parthanatos. We utilized human mammary adenocarcinoma cells (MCF7) that abundantly express the estrogen receptor alpha and beta (ERα and ERβ). Parthanatos was induced by challenging the ce...
Source: Toxicology Letters - September 30, 2014 Category: Toxicology Authors: Batnasan E, Wang R, Wen J, Ke Y, Li X, Bohio AA, Zeng X, Huo H, Han L, Boldogh I, Ba X Tags: Toxicol Lett Source Type: research

Abstract 2270: TRAIL-TZD combinatorial treatment induces apoptosis in prostate cancer cells through modulation of AMPK signaling pathway
In this study we determined AMP-activated protein kinase (AMPK) as a potential target for TRAIL-TZD-induced apoptosis in prostate cancer cells. AMPK is a family of serine/threonine protein kinase and is highly conserved from yeast to human. It consists of three subunits: a catalytic α subunit and regulatory β and γ subunits. AMPK is a well-accepted target for the treatment of metabolic syndrome and Type 2 diabetes. We used C42-DN (stably overexpressing AMPK α1-dominant negative) and C42-EV (empty vector) prostate cancer cell lines to study differences in TRAIL-TZD-induced apoptosis. Our studies showed a dose dependent ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Santha, S., Majumdar, S., Viswakarma, N., Rana, A., Rana, B. Tags: Molecular and Cellular Biology Source Type: research

Abstract 2286: Regulation of GSK3{beta} axis by combination treatment with TRAIL and Troglitazone in cancer cells
Prostate cancer is estimated to account for 29% of all new cancers and is the second leading cause of cancer-related death in men in the United States. Hormonal therapy is the only treatment for advanced forms, but androgen-independence eventually develops in most patients. Developing new treatment strategies are urgently needed, which needs a deeper molecular understanding of the events that lead to tumor progression. TNF-related apoptosis inducing ligand (TRAIL) has gained much importance recently due to its ability to preferentially induce cell death in malignant and transformed cells. However, since many tumor cells de...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Majumdar, S., Santha, S., Rana, A., Rana, B. Tags: Molecular and Cellular Biology Source Type: research