Hello Morteza Hassandokht Mashhadi

In parental MCF-7 cell line, the proliferative response at low Tamoxifen concentrations could be because of incomplete receptor binding. Tamoxifen, at low concentrations, may not fully occupy the estrogen receptor, leading to a partial agonist effect. This can result in some degree of cell proliferation, even in the presence of Tamoxifen.

Also, Tamoxifen is a selective estrogen receptor modulator (SERM). This means it can act as an agonist in some tissues and an antagonist in others. This dual behavior is tissue-specific and depends on the context of estrogen receptors in the cell, and the agonist effect is particularly observed at low concentrations.

Best,

This is an intrinsic chemoresistance. If there are some pre-deposited genetic factors present in the genome, leading expression of proteins, intracellular signaling pathways, etc., cancer cells will have a set of mechanisms that prevent or reduce effects of chemotherapeutic drugs. In addition, the interaction between the bulk of tumor and its surroundings (tumor microenvironment) render the cancer cells to respond less to the drug.

Dear Morteza

As I can guess, there is no statistically significant difference between the viability of cells in the negative control group and treated ones (50 to 1000 nM Tamoxifen). So, don't worry, no more explanation is needed. Please use one-way ANOVA, followed by an appropriate post-test to analyze the results in these cases.

Have you dissolved tamoxifen in DMSO? Low DMSO highly increases cell proliferation.