Zinc inhibits magnesium-mediated human breast cancer MDA-MB-231 cell migration on fibronectin
Bibliographic record
Abstract
Breast cancer is the most prevalent type of cancer in Canadian women and ranks second in mortality. The cause of breast cancer deaths is the tumor growth in secondary locations. Zinc has been suggested to alter the affinity by which cells attach to the extracellular matrix. The strength of cell adhesion is paramount to the ability of cancerous cells to migrate. The hypothesis for my thesis research was that zinc promotes the metastasic potential of human breast cancer cells. The overall objective of my thesis research was to characterize the effects of zinc on the growth and metastatic potential of human breast cancer cells. Breast carcinoma MDA-MB-231 cells were cultured in DMEM plus 10% Chelex-100 treated FBS supplemented with 0 (zinc-deficient medium), 5 (zinc-adequate medium), or 25 (zinc-supplemented medium) µmol/L of Zn²⁺ as ZnSO₄. After culture for 96 h, the cells were harvested for determining total cellular zinc concentration, abundance of the labile intracellular pool of zinc, and cell growth. The metastatic potential of the cells was assessed by a combination of migration rate assessed using the wound-healing assay and migration distance using the single cell migration assay. The cells were also assessed for their adhesion on fibronectin, for the involvement of specific integrin subunits using blocking antibody, and integrin activation using FACS. Zinc treatments had no effect on total cellular zinc concentration, cell growth, and viability and essentially had no effect on abundance of the labile intracellular pool of zinc. Zinc as low as 5 µmol/L inhibited MDA-MB-231 cell migration on fibronectin, reduced magnesium-mediated promotion of adhesion and thus was likely involved in inhibiting magnesium-mediated integrin activation. With the use of blocking antibodies, it was determined that α5/β1 integrin was responsible for the adhesion of the cells to fibronectin and it was likely that zinc inhibited adhesion by blocking the activation of this specific form of integrin. Together these results suggested that zinc was an inhibitor of MDA-MB-231 migration on fibronectin, and thus likely an inhibitor of metastases, contrary to the hypothesis.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".