Serk In Park
Faculty Member
Last active: 4/26/2016


The tumor microenvironment is comprised of primary cancer cells mixed with multiple types of stromal cells, of which a significant fraction originates in the bone marrow. For this reason, bone is an essential partner for tumor progression. However, it is unclear how tumor cells co-opt the bone and/or bone marrow to facilitate a favorable tumor microenvironment.

Among those bone marrow-derived cells in the tumor microenvironment, a subset of myeloid lineage cells, myeloid-derived suppressor cells (MDSCs), has been shown to correlate significantly with tumor progression. MDSCs suppress the host immune response and infiltrate tumor tissue to promote tumor growth and angiogenesis. Beyond these critical roles, little is known about the regulation of MDSCs within bone by distant primary tumor cells, not to mention therapeutic approaches targeting MDSCs.

The Park Laboratory aims to address how tumor cells stimulate the bone microenvironment to regulate MDSCs, contributing to tumor growth, angiogenesis and/or metastasis.

For this aim, prostate cancer takes a unique position, not only because of disastrous mortality and morbidity, but also because of preferential metastasis to the skeleton. Accordingly, prostate cancer cells secrete numerous important bone-modulating cytokines, leading to osteoblastic/osteolytic reactions that stimulate the adjacent bone marrow cells.

We will investigate the molecular mechanism of MDSC activation, expansion, and/or mobilization within the bone marrow of prostate tumor hosts. Additionally, we will examine the therapeutic approaches targeting MDSCs in pre-clinical models with investigational drugs. The potential research outcomes will promote understanding of the vicious partnership between cancer and bone.


The following timeline graph is generated from all co-authored publications.

Featured publications are shown below:

  1. Dissecting the role of bone marrow stromal cells on bone metastases. Buenrostro D, Park SI, Sterling JA (2014) Biomed Res Int : 875305
    › Primary publication · 25054153 (PubMed) · PMC4099112 (PubMed Central)
  2. Osteal macrophages support physiologic skeletal remodeling and anabolic actions of parathyroid hormone in bone. Cho SW, Soki FN, Koh AJ, Eber MR, Entezami P, Park SI, van Rooijen N, McCauley LK (2014) Proc Natl Acad Sci U S A 111(4): 1545-50
    › Primary publication · 24406853 (PubMed) · PMC3910564 (PubMed Central)
  3. Parathyroid hormone-related protein drives a CD11b+Gr1+ cell-mediated positive feedback loop to support prostate cancer growth. Park SI, Lee C, Sadler WD, Koh AJ, Jones J, Seo JW, Soki FN, Cho SW, Daignault SD, McCauley LK (2013) Cancer Res 73(22): 6574-83
    › Primary publication · 24072746 (PubMed) · PMC3838921 (PubMed Central)
  4. Activation of NF-kappa B signaling promotes growth of prostate cancer cells in bone. Jin R, Sterling JA, Edwards JR, DeGraff DJ, Lee C, Park SI, Matusik RJ (2013) PLoS One 8(4): e60983
    › Primary publication · 23577181 (PubMed) · PMC3618119 (PubMed Central)
  5. Signaling between transforming growth factor β (TGF-β) and transcription factor SNAI2 represses expression of microRNA miR-203 to promote epithelial-mesenchymal transition and tumor metastasis. Ding X, Park SI, McCauley LK, Wang CY (2013) J Biol Chem 288(15): 10241-53
    › Primary publication · 23447531 (PubMed) · PMC3624408 (PubMed Central)
  6. Cyclophosphamide creates a receptive microenvironment for prostate cancer skeletal metastasis. Park SI, Liao J, Berry JE, Li X, Koh AJ, Michalski ME, Eber MR, Soki FN, Sadler D, Sud S, Tisdelle S, Daignault SD, Nemeth JA, Snyder LA, Wronski TJ, Pienta KJ, McCauley LK (2012) Cancer Res 72(10): 2522-32
    › Primary publication · 22589273 (PubMed) · PMC3457788 (PubMed Central)
  7. Nuclear localization of parathyroid hormone-related peptide confers resistance to anoikis in prostate cancer cells. Park SI, McCauley LK (2012) Endocr Relat Cancer 19(3): 243-54
    › Primary publication · 22291434 (PubMed) · PMC3593272 (PubMed Central)
  8. Roles of bone marrow cells in skeletal metastases: no longer bystanders. Park SI, Soki FN, McCauley LK (2011) Cancer Microenviron 4(3): 237-46
    › Primary publication · 21809058 (PubMed) · PMC3234319 (PubMed Central)
  9. Pre-clinical mouse models of human prostate cancer and their utility in drug discovery. Park SI, Kim SJ, McCauley LK, Gallick GE (2010) Curr Protoc Pharmacol : Unit 14.15
    › Primary publication · 21483646 (PubMed) · PMC3072580 (PubMed Central)
  10. Drugs which inhibit osteoclast function suppress tumor growth through calcium reduction in bone. Li X, Liao J, Park SI, Koh AJ, Sadler WD, Pienta KJ, Rosol TJ, McCauley LK (2011) Bone 48(6): 1354-61
    › Primary publication · 21419883 (PubMed) · PMC3457787 (PubMed Central)
  11. Targeting SRC family kinases inhibits growth and lymph node metastases of prostate cancer in an orthotopic nude mouse model. Park SI, Zhang J, Phillips KA, Araujo JC, Najjar AM, Volgin AY, Gelovani JG, Kim SJ, Wang Z, Gallick GE (2008) Cancer Res 68(9): 3323-33
    › Primary publication · 18451159 (PubMed)
  12. AFAP-110 is overexpressed in prostate cancer and contributes to tumorigenic growth by regulating focal contacts. Zhang J, Park SI, Artime MC, Summy JM, Shah AN, Bomser JA, Dorfleutner A, Flynn DC, Gallick GE (2007) J Clin Invest 117(10): 2962-73
    › Primary publication · 17885682 (PubMed) · PMC1978423 (PubMed Central)
  13. Regulation of angiogenesis and vascular permeability by Src family kinases: opportunities for therapeutic treatment of solid tumors. Park SI, Shah AN, Zhang J, Gallick GE (2007) Expert Opin Ther Targets 11(9): 1207-17
    › Primary publication · 17845146 (PubMed)