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Publication

Hydroxyapatite mineral enhances malignant potential in a tissue-engineered model of ductal carcinoma in situ (DCIS).

Frank He | Nora L Springer | Matthew A Whitman | Siddharth P Pathi | Yeonkyung Lee | Sunish Mohanan | Stephen Marcott | Aaron E Chiou | Bryant S Blank | Neil Iyengar | Patrick G Morris | Maxine Jochelson | Clifford A Hudis | Pragya Shah | Jennie A M R Kunitake | Lara A Estroff | Jan Lammerding | Claudia Fischbach
Biomaterials | 2019

While ductal carcinoma in situ (DCIS) is known as a precursor lesion to most invasive breast carcinomas, the mechanisms underlying this transition remain enigmatic. DCIS is typically diagnosed by the mammographic detection of microcalcifications (MC). MCs consisting of non-stoichiometric hydroxyapatite (HA) mineral are frequently associated with malignant disease, yet it is unclear whether HA can actively promote malignancy. To investigate this outstanding question, we compared phenotypic outcomes of breast cancer cells cultured in control or HA-containing poly(lactide-co-glycolide) (PLG) scaffolds. Exposure to HA mineral in scaffolds increased the expression of pro-tumorigenic interleukin-8 (IL-8) among transformed but not benign cells. Notably, MCF10DCIS.com cells cultured in HA scaffolds adopted morphological changes associated with increased invasiveness and exhibited increased motility that were dependent on IL-8 signaling. Moreover, MCF10DCIS.com xenografts in HA scaffolds displayed evidence of enhanced malignant progression relative to xenografts in control scaffolds. These experimental findings were supported by a pathological analysis of clinical DCIS specimens, which correlated the presence of MCs with increased IL-8 staining and ductal proliferation. Collectively, our work suggests that HA mineral may stimulate malignancy in preinvasive DCIS cells and validate PLG scaffolds as useful tools to study cell-mineral interactions.

Pubmed ID: 31546097

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Associated grants

  • Agency: NCI NIH HHS, United States
    Id: P30 CA008748
  • Agency: NCI NIH HHS, United States
    Id: R01 CA173083
  • Agency: NIH HHS, United States
    Id: S10 OD012287
  • Agency: NCI NIH HHS, United States
    Id: U54 CA210184

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