Abstract
Ovarian cancer is a fatal gynecological malignancy. Although first-line chemotherapy and surgical operation are effective treatments for ovarian cancer, its clinical management remains a challenge owing to intrinsic or acquired drug resistance and relapse at local or distal lesions. Cancer stem cells (CSCs) are a small subpopulation of cells inside tumor tissues, and they can self-renew and differentiate. CSCs are responsible for the cancer malignancy involved in relapses as well as resistance to chemotherapy and radiation. These malignant properties of CSCs are regulated by cell surface receptors and intracellular pluripotency-associated factors triggered by internal or external stimuli from the tumor microenvironment. The malignancy of CSCs can be attenuated by individual or combined restraining of cell surface receptors and intracellular pluripotency-associated factors. Therefore, targeted therapy against CSCs is a feasible therapeutic tool against ovarian cancer. In this paper, we review the prominent roles of cell surface receptors and intracellular pluripotency-associated factors in mediating the stemness and malignancy of ovarian CSCs.
Highlights
Ovarian cancer has the highest mortality rate among gynecological cancers
Diagnosis at an early stage has numerous benefits such as a longer survival rate; 80% of ovarian cancer patients are diagnosed at an advanced stage (III or IV) because they exhibit no symptoms in the early stages, following which the tumor disseminates to the peritoneal cavity [2,3,4]
CD117+ ovarian cancer cells overexpress SOX2, octamer-binding transcription factor 4 (OCT4), and NANOG, which are Cancer stem cells (CSCs) markers involved in stemness and chemoresistance [45]
Summary
Ovarian cancer has the highest mortality rate among gynecological cancers. The World. Standard ovarian cancer treatment comprises first-line chemotherapy with a carboplatin-paclitaxel regimen and surgical debulking [4,6] This regimen is initially effective, recurrence is persistent owing to intrinsic or acquired chemoresistance [7,8]. Many studies have shown that there are stem-like epithelial cells in the ovarian surface [22] and fallopian tube epithelium [23]. High-grade cancer originates from the fallopian (A) and and initiation surface epithelia (B) Both normal epithelia (blue cells) haveserous a smallovarian subpopulation of stem-like cells fallopian tube (A) and surface epithelia (B). A. The stem-like cells in the fallopian tube epithelium acquire p53 mutations owing to uncertain uncertainreasons.
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