Canady Cold Plasma Conversion System Treatment: An Effective Inhibitor of Cell Viability in Breast Cancer Molecular Subtypes
Xiaoqian Cheng, Saravana R. K. Murthy, Taisen Zhuang, Lawan Ly, Olivia Jones, Giacomo Basadonna, Michael Keidar, Yasmine Kanaan, and Jerome Canady
Breast cancer is a heterogenous disease which can be classified into subtypes by the presence or absence of
estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor 2 receptor (HER2). Cold
atmospheric plasma (CAP) has been shown to be a potential treatment for cancer. In this report, a 92–99%
reduction of viability by CAP treatment was achieved across all seven tested breast cancer cell lines (p ≤ 0.05).
Increasing treatment duration and power significantly reduced breast cancer cell viability (** f(2,2) ≤ 0.0176,
*** f(5,14) ≤ 0.0033). The authors are the first to report that breast cancer sensitivity to CAP is based on receptor
status. Cells with identical receptor status showed the least difference in CAP sensitivity (p ≤ 0.05), the difference being 33% between the two ER+/PR+/HER2- cell lines (p ≤ 0.05) and 22–44% between the three
TNBC cell lines (p ≤ 0.05). HER2-negative cell lines, irrespective of ER/PR status, also showed ≤ 50% difference
in CAP sensitivity (p ≤ 0.05). Moreover, demonstration of ER-/PR-/HER2+ CAP susceptibility and ER+/PR
+/HER2+ CAP resistance suggests that ER/PR status is a significant factor in determining CAP sensitivity in
HER2-positive cells. Our novel findings on CAP sensitivity will provide insight on how to optimize CAP treatment to better overcome CAP resistance and thus prevent tumor recurrence.
estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor 2 receptor (HER2). Cold
atmospheric plasma (CAP) has been shown to be a potential treatment for cancer. In this report, a 92–99%
reduction of viability by CAP treatment was achieved across all seven tested breast cancer cell lines (p ≤ 0.05).
Increasing treatment duration and power significantly reduced breast cancer cell viability (** f(2,2) ≤ 0.0176,
*** f(5,14) ≤ 0.0033). The authors are the first to report that breast cancer sensitivity to CAP is based on receptor
status. Cells with identical receptor status showed the least difference in CAP sensitivity (p ≤ 0.05), the difference being 33% between the two ER+/PR+/HER2- cell lines (p ≤ 0.05) and 22–44% between the three
TNBC cell lines (p ≤ 0.05). HER2-negative cell lines, irrespective of ER/PR status, also showed ≤ 50% difference
in CAP sensitivity (p ≤ 0.05). Moreover, demonstration of ER-/PR-/HER2+ CAP susceptibility and ER+/PR
+/HER2+ CAP resistance suggests that ER/PR status is a significant factor in determining CAP sensitivity in
HER2-positive cells. Our novel findings on CAP sensitivity will provide insight on how to optimize CAP treatment to better overcome CAP resistance and thus prevent tumor recurrence.