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Therapy: Endocrine Therapy

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Total 38 results found since Jan 2013.

LncRNA AGPG confers endocrine resistance in breast cancer by promoting E2F1 activity
Cancer Res. 2023 Jul 18:CAN-23-0015. doi: 10.1158/0008-5472.CAN-23-0015. Online ahead of print.ABSTRACTResistance to endocrine therapy represents a major concern for patients with estrogen receptor α positive (ERα+) breast cancer. Endocrine therapy resistance is commonly mediated by activated E2F signaling. A better understanding of the mechanisms governing E2F1 activity in resistant cells could reveal strategies for overcoming resistance. Here, we identified the long non-coding RNA (lncRNA) actin gamma 1 pseudogene 25 (AGPG) as a regulator of E2F1 activity in endocrine resistant breast cancer. Expression of EGPG was inc...
Source: Cell Research - July 18, 2023 Category: Cytology Authors: Shiyi Yu Ying Wang Xue Gong Zhehao Fan Zheng Wang Zhengyan Liang Rui Wu Binjie Cao Ning Wang Caili Bi Dan Lv Haibo Sun Source Type: research

A functional genetic screen for metabolic proteins unveils GART and the de novo purine biosynthetic pathway as novel targets for the treatment of luminal A ER α expressing primary and metastatic invasive ductal carcinoma
In conclusion, GART inhibition by LMX or other inhibitors of the de novo purine biosynthetic pathway could be a novel effective strategy for the treatment of primary and metastatic BCs.
Source: Frontiers in Endocrinology - April 18, 2023 Category: Endocrinology Source Type: research

JMJD6 orchestrates a transcriptional program in favor of endocrine resistance in ER+ breast cancer cells
High expression of Jumonji domain containing protein 6 (JMJD6) is strongly associated with poor prognosis in estrogen receptor positive (ER+) breast cancer. We overexpressed JMJD6 in MCF7 cells (JOE cells) and performed RNA-seq analysis. 76% of differentially expressed genes (DEGs) overlapped with ER target genes. Pathway analysis revealed that JMJD6 upregulated a larger subset of genes related to cell proliferation as compared to ER. Interestingly, JOE cells showed a decrease in ER target gene expression prompting us to check ER levels. Indeed, JOE cells showed a significant decrease in both ESR1 and ER levels and JMJD6 s...
Source: Frontiers in Endocrinology - November 7, 2022 Category: Endocrinology Source Type: research

Cancers, Vol. 14, Pages 2380: Endocrine Therapy-Resistant Breast Cancer Cells Are More Sensitive to Ceramide Kinase Inhibition and Elevated Ceramide Levels Than Therapy-Sensitive Breast Cancer Cells
In this study, we have investigated how alterations in sphingolipids promote cell survival in ET-resistant breast cancer. We have performed LC-MS-based targeted sphingolipidomics of tamoxifen-sensitive and -resistant MCF-7 breast cancer cell lines. Follow-up studies included treatments of cell lines and patient-derived xenograft organoids (PDxO) with small molecule inhibitors; cytometric analyses to measure cell death, proliferation, and apoptosis; siRNA-mediated knockdown; RT-qPCR and Western blot for gene and protein expression; targeted lipid analysis; and lipid addback experiments. We found that tamoxifen-resistant cel...
Source: Cancers - May 12, 2022 Category: Cancer & Oncology Authors: Purab Pal Alec Millner Svetlana E. Semina Rosemary J. Huggins Logan Running Diana S. Aga Debra A. Tonetti Rachel Schiff Geoffrey L. Greene G. Ekin Atilla-Gokcumen Jonna Frasor Tags: Article Source Type: research

Clinically relevant CHK1 inhibitors abrogate wild-type and Y537S mutant ER α expression and proliferation in luminal primary and metastatic breast cancer cells
CONCLUSIONS: CHK1 could be considered as an appealing novel pharmacological target for the treatment of luminal primary and MBCs.PMID:35418303 | DOI:10.1186/s13046-022-02360-y
Source: Clinical Breast Cancer - April 14, 2022 Category: Cancer & Oncology Authors: Sara Pescatori Stefano Leone Manuela Cipolletti Stefania Bartoloni Alessandra di Masi Filippo Acconcia Source Type: research

Knockdown of YAP/TAZ sensitizes tamoxifen-resistant MCF7 breast cancer cells
In conclusion, targeting the YAP/TAZ-PSAT1 axis could sensitize tamoxifen-resistant MCF7 breast cancer cells by modulating the mTORC1-survivin axis.PMID:35231654 | DOI:10.1016/j.bbrc.2022.02.083
Source: Biochemical and Biophysical Research communications - March 1, 2022 Category: Biochemistry Authors: Yu Jin Kim Se-Kyeong Jang Sung-Eun Hong Chan Sub Park Min-Ki Seong Hyun-Ah Kim Ki Soo Park Chun-Ho Kim In-Chul Park Hyeon-Ok Jin Source Type: research

Targeting CDK7 reverses tamoxifen resistance through regulating stemness in ER+ breast cancer
CONCLUSION: Our data indicate, for the first time, that CDK7-targeted therapy in ER+ breast cancer ameliorates tamoxifen resistance, at least in part, by inhibiting cancer stemness. Thus, targeting CDK7 might represent a potential approach for relieving tamoxifen resistance in ER+ breast cancer.PMID:35000145 | DOI:10.1007/s43440-021-00346-9
Source: Pharmacological Reports - January 9, 2022 Category: Drugs & Pharmacology Authors: Yasmin M Attia Salama A Salama Samia A Shouman Cristina Ivan Abdelrahman M Elsayed Paola Amero Cristian Rodriguez-Aguayo Gabriel Lopez-Berestein Source Type: research

Cancers, Vol. 13, Pages 3612: Estrogen Receptor-Alpha and p53 Status as Regulators of AMPK and mTOR in Luminal Breast Cancer
. Das Luminal breast cancer (LBC) driven by dysregulated estrogen receptor-alpha (ERα) signaling accounts for 70% of the breast cancer cases diagnosed. Although endocrine therapy (ET) is effective against LBC, about one-third of these patients fail to respond to therapy owing to acquired or inherent resistance mechanisms. Aberrant signaling via ERα, oncogenes, growth factor receptors, and mutations in tumor suppressors such as p53 impinge on downstream regulators such as AMPK and mTOR. While both AMPK and mTOR have been reported to play important roles in determining sensitivity of LBC to ET, how the ERα-p53 crossta...
Source: Cancers - July 19, 2021 Category: Cancer & Oncology Authors: Nishant Gandhi Chetan C. Oturkar Gokul M. Das Tags: Article Source Type: research

Overexpression of TMEM47 Induces Tamoxifen Resistance in Human Breast Cancer Cells
CONCLUSIONS: Our results suggest that overexpression of TMEM47 in MCF-7 cells acquired TAM resistance to those cells, and knockdown of TMEM47 in TAMR/MCF-7 cells reversed their resistance to TAM. TMEM47 might confer TAM resistance on MCF-7 cells through the inhibition of apoptosis.PMID:33745390 | DOI:10.1177/15330338211004916
Source: Technology in Cancer Research and Treatment - March 22, 2021 Category: Cancer & Oncology Authors: Xin Men Mengyang Su Jun Ma Yueyang Mou Penggao Dai Chao Chen Xi An Cheng Source Type: research

PELP-1 regulates adverse responses to endocrine therapy in Estrogen Receptor (ER) positive breast cancer.
CONCLUSIONS: Our data confirms previous reports that anti-estrogens induce an adverse cell phenotype in ER+ breast cancer, particularly in the absence of homotypic cell contact. These results implicate E-cadherin and PELP-1 as potential biomarkers when deciding upon optimum adjuvant endocrine therapy, whereby tumours with high PELP-1/low E-cadherin expression may benefit from estrogen withdrawal therapy via aromatase inhibition, as opposed to ER modulation/antagonism. PMID: 33473257 [PubMed]
Source: Oncotarget - January 23, 2021 Category: Cancer & Oncology Tags: Oncotarget Source Type: research