Table 1.

Derivation, p53 and other genomic mutations of breast cancer cell lines used in this study

										p53 mutation
Cell lines	Growth properties	Gene cluster	ER	PR	HER2	Tumor type	Age(years)	Ethnicity	P53 status	Nature	Site	cDNA discription	Protein	Functional impact	Other genomic alterations
MCF-7	Adherent	Luminal	+	+	–	Adenocarcinoma	69	white	WT						CDKN2A; PIK3CA
ZR-75–1	Adherent	Luminal	+	–	–	IDC	63	white	WT						–
SK-BR-3	Adherent	HER2 +	–	–	+	Adenocarcinoma	43	white	MUT	Missense mutations	5-exon	c.524G > A	p.R175H	Chemoresistance; Angiogenesis; Inflammatory response; Metabolic reprogramming; Genetic Instability; Tumor Cell proliferation; Migration, Invasion and Metastasis	–
DU4475	Suspension	TNBC	–	–	–	Carcinoma	70	white	WT						APC; BRAF; RB1
MB-231	Adherent	TNBC	–	–	–	Adenocarcinoma	51	white	MUT	Missense mutations	8-exon	c.839G > A	p.R280K	Chemoresistance; Angiogenesis; Inflammatory response	BRAF; CDKN2A; RAS
HS578T	Adherent	TNBC	–	–	–	Carcinoma	74	white	MUT	Missense mutations	5-exon	c.469G > T	p.V157F	A novel transcriptome regulation	–
HCC1937	Adherent	TNBC	–	–	–	IDC	23	white	MUT	Nonsense mutations	8-exon	c.916C > T	p.R306*		BRCA1

ER Estrogen receptor, IDC Invasive ductal carcinoma, PR Progestogen receptor, TNBC Triple-negative breast cancer, WT Wild type, MUT Mutant type