LKB1 expression is inhibited by estradiol-17β in MCF-7 cells

  title={LKB1 expression is inhibited by estradiol-17$\beta$ in MCF-7 cells},
  author={Kristy A. Brown and Kerry J. McInnes and Kiyoshi Takagi and Katsuhiko Ono and Nicole I. Hunger and Lin Wang and Hironobu Sasano and Evan R. Simpson},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},
  • K. BrownK. McInnes E. Simpson
  • Published 1 November 2011
  • Biology, Medicine
  • The Journal of Steroid Biochemistry and Molecular Biology

Expression of STK11 gene and its promoter activity in MCF control and cancer cells

This study for the first time relates the altered STK11 gene expression in breast cancer cells with altered promoter activity to shed light on the new therapeutic approaches against breast cancer by targeting gene or its promoter.

The transcriptional responsiveness of LKB1 to STAT-mediated signaling is differentially modulated by prolactin in human breast cancer cells

LKB1 is differentially regulated by PRL at the level of transcription in representative human breast cancer cells, and the cellular estrogen receptor status may affect PRL-responsiveness.

Clinical Relevance of Liver Kinase B1(LKB1) Protein and Gene Expression in Breast Cancer

The study results indicate that LKB1 expression is not prognostic in the whole population of breast cancer patients, but it is a potential predictor of OS in the subset of HER2-positive patients.

JAK2/STAT and LKB1: An interaction linking PRL-mediated metabolic changes and structural integrity in MDA-MB-231 human breast cancer cells

The association between JAK2 and LKB1, the metabolic effects linked to JAK1/LKB1-mediated signaling elicited by PRL in MDA-MB-231 cells, and interplay between several important intracellular signaling networks that regulate both metabolism and cell polarity merit further investigation in an extended panel of cells, as well as patient-derived samples.

Adenosine monophosphate activated protein kinase (AMPK), a mediator of estradiol-induced apoptosis in long-term estrogen deprived breast cancer cells

Results reveal that AMPK is an important factor mediating E2-induced apoptosis in LTED cells, which is implicative of therapeutic potential for relapsing breast cancer after hormone therapy.

MicroRNA-17 promotes normal ovarian cancer cells to cancer stem cells development via suppression of the LKB1-p53-p21/WAF1 pathway

It is suggested that mature miR-17 expression may have an important role in the pathogenesis of human ovarian tumors through its interference with the LKB1-p53-p21/WAF1 pathway expression by epigenetic modification.

JAK 2 / STAT and LKB 1 : an interaction linking PRL-mediated metabolic changes and structural integrity in MDA-MB-231 human breast cancer cells

A novel interaction between JAK2 and LKB1 is established and phosphorylation/activation of STAT3 and STAT5 were differentially affected by WP1066 pre-treatment, which is of relevance in gaining a better understanding of the epithelial-to-mesenchymal transition (EMT) and mechanisms that protect aggressive cancer cells.

Endocrine-related cancers and the role of AMPK

Low LKB1 Expression Results in Unfavorable Prognosis in Prostate Cancer Patients

The expression of LKB1 was lower in PCa tissues and might be a predictor for the prognosis of PCa patients and Cox regression analysis confirmed that L KB1 could be regarded as a prognostic biomarker for PCa Patients.



Important role of the LKB1-AMPK pathway in suppressing tumorigenesis in PTEN-deficient mice.

The results demonstrate the potential of AMPK activators, such as clinically approved metformin, as anticancer agents, which will suppress tumour development by triggering a physiological signalling pathway that potently inhibits cell growth.

[Function and prognostic value of tumor suppressor gene LKB1 in human breast carcinoma].

Reintroducing L KB1 into breast cell of the lines lacking LKB1 expression restores LKB 1 activity and induces growth suppression by G(1) cell cycle block.

Histological evaluation of AMPK signalling in primary breast cancer

Reduced signalling via the AMPK pathway, and the inverse relationship with histological grade and axillary node metastasis, suggests that AMPK re-activation could have therapeutic potential in breast cancer.

Metformin inhibits aromatase expression in human breast adipose stromal cells via stimulation of AMP-activated protein kinase

Results suggest that metformin would reduce the local production of estrogens within the breast thereby providing a new key therapeutic tool that could be used in the neoadjuvant and adjuvant settings and conceivably also as a preventative measure in obese women.

LKB1 is recruited to the p21/WAF1 promoter by p53 to mediate transcriptional activation.

It is found that, consistent with previous studies, LKB1 stabilizes p53 in vivo, correlating with activation of p21/WAF1 and directly or indirectly phosphorylates p53 Ser15 (previously shown to be phosphorylated by AMP-dependent kinase) and p53Ser392, required for L KB1-dependent cell cycle G(1) arrest.

Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells.

It is shown here that metformin acts as a growth inhibitor rather than an insulin sensitizer for epithelial cells, which provides evidence for a mechanism that may contribute to the antineoplastic effects of met formin suggested by recent population studies and justifies further work to explore potential roles for activators of AMP kinase in cancer prevention and treatment.

Increased lipogenesis in cancer cells: new players, novel targets

Not only fatty acid synthase, but in fact all key enzymes involved in fatty acid synthesis as well as key metabolic regulators are potential targets for antineoplastic intervention.

LKB1 Protein Expression in Human Breast Cancer

Although frequent methylation of the L KB1 gene has been reported in papillary carcinomas of the breast, the authors did not find loss of protein expression in these lesions and found LKB1 gene methylation in several of these invasive carcinomas.

LKB1-dependent signaling pathways.

The data suggest that LKB1 functions as a tumor suppressor by not only inhibiting proliferation, but also by exerting profound effects on cell polarity and, most unexpectedly, on the ability of a cell to detect and respond to low cellular energy levels.