Table 2 Effect of myocardial infarction and cardiac hypertrophy on tumor progression: Evidence from in vivo studies
Model | Cardiac changes | Plasma biomarker changes | Tumor status | Interpretation | Refs. | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
LV function | LVH | Fibrosis | mRNA expression | Protein and immune | Cancer type | Growth | Metastasis | mRNA expression and immune | |||
MI-induced HF APCmin mice | ↓ | ↑ | ↑ | ↑SerpinA3, SerpinA1, FN, CP, PON1, CTGF | – | Colon | ↑ | – | – | HF enhanced colon cancer growth irrespective of hemodynamics through cardiac excreted factors | [16] |
Heterotopic heart transplant of MI heart in APCmin mice into APCmin mice | ↔ | ↑ | ↑ | ↑SerpinA3, FN, PON1  ↔ SerpinA1, CP | – | Colon | ↑ | – | – | ||
MI-induced HF mice with xenograft LLC | ↓ | – | – | ↑miR-22-3p, pre-mi-R-22 | ↑miR-22-3p | Lung | ↑↑ | – | ↑miR-22-3p ↔pre-mi-R-22 | MI-induced HF enhanced tumor growth by attenuation of tumor sensitivity to ferroptosis via miR-22-3p | [18] |
MI-induced HF mice with xenograft LLC + erastin 30 mg/kg/IP/OD | ↓ | – | – | – | – | Lung | ↑ | – | – | ||
MI-induced HF mice with xenograft LLC + IKE 30 mg/kg/IP/OD | ↓ | – | – | – | – | Lung | ↑ | – | – | ||
Xenograft LLC mice + erastin 30 mg/kg/IP/OD | ↔ | – | – | – | – | Lung | ↓↓ | – | – | ||
Xenograft LLC mice + erastin 30 mg/kg/IP/OD + Sham-EXO/Intra-tumor/q 48 h | ↔ | – | – | – | – | Lung | ↓↓ | – | – | ||
Xenograft LLC mice + erastin 30 mg/kg/IP/OD + Sham-EXO/Intra-tumor/q 48 h | ↓ | – | – | – | – | Lung | ↓ | – | – | ||
MI-induced HF in inhibited cardiomyocyte specific miR-22-3p mice with xenograft LLC + erastin 30 mg/kg/IP/OD | ↓ | – | – | ↓ miR-22-3p | ↓ miR-22-3p | Lung | ↓ | – | ↓ miR-22-3p | ||
TAC-induced pressure overload mice with orthotopic breast cancer (PyMT) | ↓ | ↑ | ↔ | ↑periostin, CTGF | ↑periostin, CTGF ↔CD8+ T cell | Breast | ↑ | ↔ | ↔CD8+ T cell | Early cardiac remodeling increased breast and lung cancer growth and metastasis possibly via periostin and CTGF | [23] |
TAC-induced pressure overload mice + PyMT injection | ↓ | ↑ | ↔ | ↑periostin, CTGF | ↑periostin, CTGF | Breast | – | ↑ | – | ||
TAC-induced pressure overload mice with xenograft lung cancer (LLC) | ↓ | ↑ | ↔ | ↑periostin, CTGF | ↑periostin, CTGF ↔CD8+ T cell | Lung | ↑ | ↔ | ↔CD8+ T cell | ||
TAC-induced pressure overload mice + LLC injection | ↓ | ↑ | ↔ | ↑periostin, CTGF | ↑periostin, CTGF | Lung | – | ↑ | – | ||
TAC-induced pressure overload NOD/SCID mice with orthotopic breast cancer | ↓ | ↑ | ↔ | ↑periostin, CTGF | ↑periostin, CTGF | Breast | ↑ | – | – | ||
TAC-induced pressure overload MCRR mice with orthotopic breast cancer | ↔ | ↔ | – | ↔periostin, CTGF | ↔periostin, CTGF | Breast | ↔ | – | – | ||
Low-dose PE induced hypertension mice with orthotopic breast cancer (PyMT) | ↔ | ↑ | ↑ | ↑periostin, FN ↔CTGF, SerpinA3, SerpinE1, PON1, CP | ↑periostin, FN, CTGF | Breast | ↑ | – | ↑CTGF ↔periostin, FN, SerpinA3, SerpinE1, PON1, CP | Cardiac remodeling in the absence of contractile dysfunction was sufficient to promote breast cancer growth | [25] |
ATF3-transgenic mice with orthotopic breast cancer (PyMT) | ↓ | ↑ | ↑ | ↑periostin, SerpinA3, SerpinE1, CP, CTGF, FN | ↔CP, CTGF, FN | Breast | ↑ | – | ↑CTGF, FN ↔SerpinA3 | Cardiac remodeling promoted tumor growth in ATF3-transgenic mice with breast and lung cancer models | [24] |
ATF3-transgenic mice + PyMT injection | – | – | – | – | – | Breast | – | ↑ | – | ||
ATF3-transgenic mice with xenograft LLC | ↓ | ↑ | – | – | – | Lung | ↑ | – | – | ||
ATF3-transgenic mice with orthotopic breast cancer + doxycycline | – | ↑ | – | – | – | Breast | ↑ | – | – | ||
ATF3-transgenic mice + doxycycline + PyMT injection | – | – | – | – | – | Breast | – | ↑ | – | ||
MI-induced mice with orthotopic breast cancer (E0771) | ↓ | ↑ | – | – | ↑Ly6Chi monocyte | Breast | ↑ | – | ↑Ly6Chi monocyte ↓T cells ↑Treg cells | MI enhanced tumor growth in breast cancer mice model via reprogramming of myeloid cells toward immunosuppressive state | [17] |
CD45.2 mice implanted E0771 tumor + isolated Ly6Chi monocytes from MI-induced CD45.1 non-tumor bearing mice | – | – | – | – | – | Breast | ↔ | – | ↔Ly6Chi CD45.1 | ||
MI-induced CD45.2 mice implanted E0771 tumor + isolated Ly6Chi monocytes from naive CD45.1 non-tumor bearing mice | – | – | – | – | – | Breast | ↔ | – | ↑Ly6Chi CD45.1 | ||
MI-induced CCR2DTR mice implanted E0771 tumor + DT injection (vs MI WT) | – | – | – | – | ↓Ly6Chi monocyte | Breast | ↓ | – | ↓Ly6Chi monocytes ↓Treg cells ↑CD8+ T cell ↑CD8+GrB+ | ||
Sham-operated CCR2DTR mice implanted E0771 tumor + DT injection | – | – | – | – | ↓Ly6Chi monocyte | Breast | ↔ | – | ↓Ly6Chi monocytes  ↔ Treg cells ↑CD8+ T cell  ↔ CD8+GrB+ | ||
MI-induced mice implanted E0771 tumor + anti-CD8 | – | – | – | – | – | Breast | ↔ | – | ↓T cells | ||
Sham-operated mice implanted E0771 tumor + anti-CD8 | – | – | – | – | – | Breast | ↔ | – | ↓T cells | ||
CD45.1 mice + BM transplant from MI-induced CD45.2 mice implanted E0771 tumor + implanted E0771 after BM transplant (vs sham) | – | – | – | – | ↑Ly6Chi monocytes | Breast | ↑ | – | – | ||
MI-induced MMTV-PyMT mice | – | – | – | – | – | Breast | ↑ | ↑ | ↑Ly6Chi monocytes ↔ T cells  ↔ Treg cells | ||
MI-induced HF mice with orthotopic renal cancer (Renca cells) | ↓ | ↑ | ↑ | – | – | Renal | ↔ | ↔ | – | HF had neutral effect on renal cancer cell growth in MI-induced HF mice model | [19] |