Despite a century of cancer research the cause of breast cancer remains unknown. Age, diet, stress, hormone factors, genetic predisposition, and cancer viruses are all suspected as possible causative factors, but totally ignored are infectious bacteria which have been implicated in breast cancer and...
ATRIM56 depletion inhibits the cell proliferation in breast cancer cells. MCF-7 cells were transfected with 50 nM TRIM56 siRNA (mix of #1 and #2) or 50 nM control siRNA. After 24 h, the WST assay was used to determine the cellular metabolic activity at indicated time points after...
α status was essential to the function of OTUD7B in breast carcinogenesis. In conclusion, our study revealed an interesting post-translational mechanism between ERα and OTUD7B in ERα-positive breast cancer. Targeting the OTUD7B–ERα complex may prove to be a potential approach to treat pa...
Overexpression of YAP1 in estrogen-treated breast cancer cells and human breast tissues To investigate the effect of E2 treatment on YAP1 expression in breast cancer cells, MCF7 cells were treated with E2 at 5, 10, and 20 nM for 2, 4, 8, and 24 h. As shown in Figure 1A, E2 treatm...
This was not surprising to me, as excess estrogen has also been linked to thyroid cancer. Here is the connection. Remember how estrogen and progesterone work as opposites and provide balance? Well, estrogen suppresses thyroid hormone and increases our need for TSH, while progesterone stimulates ...
Nazmeen A, Chen G, Ghosh TK, Maiti S (2020a) Breast cancer pathogenesis is linked to the intra-tumoral estrogen sulfotransferase (hSULT1E1) expressions regulated by cellular redox dependent Nrf-2/NFκβ interplay. Cancer Cell Int 20:70 Article PubMed PubMed Central CAS Google Scholar Naz...
Most of the nongenomic responses of E2 have been linked to ERα36, a 36-kDa splice variant of ERα66 (9., 8., 9., 10., 11., 12., 13., 14., 15.) that is mainly expressed on the plasma membranes of breast cancer cells, particularly in TNBC (15, 16). ERα36 has a novel...
Therefore, restoring estrogen to youthful levels through ERT can significantly boost immune function and prevent fatal illnesses related with advancing age. An increasing number of scientific evidence supports the “immune-boosting” effect of estrogen: In patients with early breast cancer, ERT does not...
These findings further support the hypothesis of bi-directional crosstalk between the ER and HER2 pathways in breast cancer, which can lead to the activation of an alternative “escape” survival pathway (e.g., ER signaling) that gives rise to the development of acquired treatment resistance. Mor...
C-Y Lin3, Y Qiao1, K Zendehdel2, S Stro¨ mblad1, E Treuter1 and K Dahlman-Wright1 Estrogen receptor a (ERa) is initially expressed in the majority of breast cancers and promotes estrogen-dependent cancer progression by regulating the transcription of genes linked to cell proliferation. ...