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Figure 2. Centrosome duplication cycle. Centrosome duplication begins at the G1-S transition, with the disengagement of the pair of
centrioles. Plk4 binds and phosphorylates STIL and associates with SAS-6. Thus, the cartwheel forms the proximal wall of the mother
centriole. Other proteins are recruited to the cartwheel and the new daughter centriole (procentriole) begins to grow from the existing
centrioles during S and reaches the full length at the G2 phase. Duplicated centrosomes separate at the beginning of the M phase, helped
by kinases NEK2a and Plk1. PCM mature and the cartwheels disassemble in the early M phase. After the separation of two daughter cells,
each cell inherits one centrosome. The figure is adapted and modified [15]

Table 1. Association of centrosome proteins with epigenetic disturbances in different types of tumors
Cancer marker Cancer types Ref.
USP9X Breast [34]
BRCA1 Breast [32]
p53 Breast [33]
Cep70 Pancreatic [35]
Pericentrin Breast, bladder [36,37]
Nek2 Prostate, breast, melanoma [38-40]
TACC3 Gastric, melanoma, ovarian [41-43]
Plk4 Breast, melanoma [44,45]
Aurora A Esophageal [46]
CTCF Breast [47]

These studies indicate that centrosome aberrations not only produce aneuploidy, chromosome instability
leading to tumorigenesis but also promote cancer drug resistance.

MECHANISMS OF CANCER DRUG RESISTANCE INVOLVING CENTROSOME
The mechanism underlying chemo-resistance (mitotic drug resistance) is not yet clear. Several studies
provide insights into the molecular basis of centrosome abnormalities that produce drug resistance, either