Table 1.

Transcription factors in chemo-resistance.

Transcription Factors	Chemo-Resistance Mechanism	Cancer Type	Drug	Reference
NF-κB	p50 subunit of NF-κB associate with BRCA1 on the promoter of genes encoding anti-apoptotic proteins to promote BRC1-mediated resistance to DNA damage	Breast cancer	Etoposide and Camptothecin	[185]
	p65/RelA activation in 267B1/K-ras overexpressing tumorigenic cells promote chemo-resistance	Prostate cancer	Trichostatin A	[186]
	NF-κB regulates MDR1 gene expression	Colon cancer	Daunomycin	[187]
AP1	The AP-1 family member JunB promoted growth and dexamethasone-resistance in multiple myeloma cells. These were reversed by the silencing of JunB.	Multiple myeloma cell	Dexamethasone	[188]
	c-Jun upregulated FoxM1 in sorafenib-resistant liver cancer cells. Knocking down c-jun expression reversed this, resulting in enhanced sensitivity of cells to sorafenib.	Liver cancer	Sorafenib	[189]
	Activation of AP-1 expression induced transcription of XIAP conferring resistance to chemotherapeutics	Breast and liver cancer cells	HDAC inhibitor, JNJ-2648158	[190]
STAT3	Expression of pSTAT3 was higher in cisplatin-resistant cells and silencing of STAT3 increased chemotherapy sensitivity	Ovarian cancer	Cisplatin	[191]
	Activation of STAT3 in association with p53/RAS pathway controls metastasis and cisplatin-resistance. This also involves Slug, MAPK and PI3K/AKT axes.	Ovarian cancer	Cisplatin	[192]
	ID1 mediates resistance via STAT3-mediated induction of ATF6 transcription to induce autophagy	Ovarian cancer	Paclitaxel and cisplatin	[193]
	Involvement of Src/STAT3 signaling pathway in chemotherapy resistance	Triple negative breast cancer	Camptothecin, Doxorubicin	[194]
HIF-1	HIF-1 induced carbonic anhydrase IX expression. Inhibition of carbonic anhydrase IX restored chemo-sensitivity against vinorelbine	Lung cancer	Vinorelbine	[195]
	HIF-2α overexpression increased the expression of stem cell markers (c-Myc, OCT4, Nanog) and Paclitaxel-resistance. These were accomplished via activation of Wnt and Notch pathways.	Breast cancer	Paclitaxel	[196]
	Treatment of breast cancer cell lines with Paclitaxel or Gemcitabine increased HIF activity. This in turn enriched the cancer stem cell population and increased the expression of multidrug resistance 1 (MDR1)	Breast cancer	Paclitaxel or Gemcitabine	[70]
	HIF-dependent BMX kinase upregulation resulted in therapeutic resistance through a compensatory pro-survival signaling mechanism	Acute myeloid leukemia	Sorafenib	[197]
	HIF2 and COX2 activated Snail and downregulated E-cadherin expression to promote invasion and resistance to sorafenib	Renal cancer	Sorafenib	[198]
	HIF-2α activated TGF-α/EGFR pathway to promote proliferation and sorafenib-resistance, which was antagonized by HIF-2α siRNA	Hepatocellular carcinoma	Sorafenib	[199]
MYC	MYC cooperated with MCL1 to increase mitochondrial oxidative phosphorylation and ROS to maintain CSCs and promote chemo-resistance	Triple negative breast cancer	Paclitaxel	[200]
	c-Myc promoted the self-renewal, tumorigenicity, invasion and drug-resistance of colon CSCs	Colon cancer	5-Fluorouracil, Oxaliplatin, FOLFOX	[201]
	c-Myc upregulated tongue cancer resistance-associated protein 1 (TCRP1) to promote chemoresistance, and this axis acted as a negative biomarker of prognosis	Tongue and lung cancer	Cisplatin	[202]
	Overexpression of c-Myc promoted resistance to chemotherapeutic drugs, increased colony formation and inhibited cell differentiation	Acute Myeloid Leukemia Cells	Cytarabine (Ara-C), Daunomycin, Doxorubicin	[203]
ETS1	ETS1 upregulated MDR1 and MMP9 expressions to promote paclitaxel-resistance and invasion	Hormone-refractory prostate cancer	Paclitaxel	[204]
	ETS1 promoted cisplatin-resistance by transcriptional activation of genes involved in reducing cisplatin toxicity, including metallothioneins and DNA repair enzymes	Ovarian cancer	Cisplatin	[205]
	ETS1 binding to Pregnane X receptor (PXR) increases the transcriptional activity of PXR, leading to sorafenib-resistance through induction of multi-drug resistance genes	Hepatocellular carcinoma	Sorafenib	[109]
	ETS1 increased MDR1 expression, and siRNA-mediated silencing of ETS1 reduced MDR1 expression and effectively reversed drug-resistance	Adriamycin-resistant breast cancer cells	Adriamycin	[206]
β-catenin/TCF	Leucine-rich-repeat-containing G protein-coupled receptor (LGR) promoted stemness and chemo-resistance via activating Wnt/β-catenin signaling pathway	Ovarian cancer	Cisplatin and Paclitaxel	[207]
	β-catenin promoted survival of metastatic melanoma cells and not benign melanocytes or primary, non-invasive melanoma cells. Downregulation of β-catenin sensitized metastatic melanoma cells towards chemotherapy	Metastatic melanoma cells	Temozolomide, Cisplatin and Doxorubicin	[208]
	Prospero-related homeobox 1 (PROX1) upregulated β-catenin transcription and nuclear translocation to activate the Wnt/β-catenin pathway in HCC, which lead to high proliferation and sorafenib-resistance	Hepatocellular carcinoma	Sorafenib	[209]
	Nek2 stabilized β-catenin, increased its nuclear translocation, and activated the transcription of its downstream target genes, to promote sorafenib-resistance	Hepatocellular carcinoma	Sorafenib	[210]
	Suppression of checkpoint kinase 1 (CHK1) pathway by Wnt/β-catenin in p53 wild-type colorectal cancer cells, promoted drug-resistance	Colorectal cancer	5-Fluorouracil	[211]
Transcription factors related to stemness (Oct-4, Sox-2, Nanog)	Chemotherapy-induced Oct-4 expression promoted acquired resistance in cancer	Bladder cancer	Cisplatin	[212]
	High expression of Oct-4 in CD133+CSCs maintained self-renewal and drug-resistance in lung cancer. Knocking down Oct-4 expression in CD133+CSCs significantly inhibited tumor invasion and colony formation, and increased apoptosis	Lung cancer	Cisplatin, Etoposide, Doxorubicin, and Paclitaxel	[213]
	HDAC11-mediated increase in expression of Sox2 is required for the maintenance of CSCs to promote drug resistance	Lung adenocarcinoma	Cisplatin, Erlotinib and Gefitinib	[214]
	IL-6/p-STAT3 activation increased the expression of DNMT3b/OCT4 which conferred early recurrence and poor prognosis in HCC	Hepatocellular carcinoma	Sorafenib	[215]
	The expression of Sox2 and CD24 were upregulated in targeted-therapy resistant melanoma cells, which was mediated by activated STAT3. Activation of STAT3, Sox2 and CD24 promoted adaptive-resistance to BRAF inhibitors.	Melanoma	BRAF inhibitors (Vemurafenib, plx8394 and pIx7904)	[216]
	Increased expression of Oct-4 and Nanog play important roles in the proliferation, migration, invasion and chemoresistance of pancreatic CSCs, and might serve as important prognostic biomarkers and therapeutic targets for pancreatic cancer.	Pancreatic cancer	Gemcitabine	[217]