Stem Cell Biomarkers and their mechanisms in Prostate Cancer

Present there is little effective treatment available for castration resistant prostate cancer (PCa), which is the cause for most of prostate cancer related deaths. Emerging evidence suggested that cancer stem cells might play an important role in resistance to traditional cancer therapies, and the studies of cancer stem cells (including specific isolation and targeting on those cells) might benefit the discovery of novel treatment of prostate cancer, especially castration resistant disease.

Standard PCa treatment includes radical prostatectomy, radiotherapy, chemotherapy and castration (either by drug or by surgery, mainly for androgen sensitive PCa), as well as immunotherapy and palliative therapy (mainly for castration resistant PCa (CRPC)). CRPC is responsible for majority of the PCa-related deaths, and currently there are two major hypotheses of CRPC carcinogenesis, the adaptive mechanism and the selective mechanism. The adaptive mechanism suggests gene mutations in PCa cells (e.g., mutations of androgen receptor (AR)), dysregulated expression of genes, etc., contribute to CRPC development. The selective mechanism, which is emerged in the last few decades, suggests that pre-existing castration-resistant sub clones in primary PCa tissues and cancer stem cell selection dominates CRPC development. Recently, it has been suggested that stem-cell directed differentiation therapy could promote differentiation of cancer stem cells and sensitize them to anticancer drugs (such as synergistic androgen signalling blocking agents).

The mechanism and pathway map of the prostate cancer. Solid line between genes/molecules indicates direct regulation, while dashed lines indicates possible indirect regulation. Circle indicates a group of similar molecules.

Cancer stem cells (CSCs) were defined as cells with capacity of self-renewal and proliferation in cancer tissue. Over years, scientists have been arguing about the origin of cancer stem cells. CSCs were suggested to originate from mutated normal stem cells, from mutated progenitor cells in the process of differentiation which re-gains the characteristics of stem cells, or from mature cells that re-acquired self-renewal ability.

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