Table 1.

Overexpression of the long non-coding RNA H19 in several cancer

Type of cancer	Known inducers of H19 overexpression	Biological consequences and/or clinical values	References
Glioma	/	• Increase of cell proliferation • Enhancement of pro-angiogenic factors • Inverse correlation with patient’s survival rate	[29] [30] [31]
Oral squamous cell carcinoma	/	• Increase of cell proliferation • Promotion of migration and invasion through epithelial-to-mesenchymal (EMT)-associated protein expression regulation • Immune escape through modulation of pro- and anti-immune factors expression	[32] [33, 34] [35]
Lung adenocarcinoma	• Cisplatin treatment • Benzo[α]pyrene treatment • HGF/SF	• Acquisition of chemoresistance • Disruption of genomic stability by increased mutation frequency. • Association with patients’ clinical resistance to cisplatin-based chemotherapy • Serological marker for patients’ auxiliary diagnosis • Activation of migration and invasion	[36] [37] [38] [39]
Breast cancer	• E2F1 • ERα/17β-estradiol • 91H • HGF • TGF- β • Hypoxia	• Increase of cell proliferation • Paclitaxel resistance through epigenetic silencing of pro-apoptotic genes • Enhancing of cell migratory potential • Potential biomarker for early screening and prognosis monitor • Induction of epithelial-to-mesenchymal transition	[29, 40–42] [43] [44] [45] [46] [39]
Gastric cancer	• c-Myc • PEG10	• Inhibition of growth suppressors activity • Inhibition of pro-apoptotic genes expression • Promotion of cell migration, invasion, and metastasis • Correlation with poor prognosis and clinical stage • Potential biomarker for diagnosis and early tumor screening	[47, 48] [49] [50] [51] [52]
Liver cancer	• Cyclin D/CUDR • EGR1/PKM2 • Bcl2 • TNF-α • TGF-β	• Inhibition of growth suppressors expression • Modulation of telomerase activity • Activation of pro-angiogenic factors expression • Regulation of immunological response • Association with bile acid homeostasis deregulation • Enhancement of obstructive cholestatic liver fibrosis development • Induction of epithelial-to-mesenchymal transition	[53] [54] [55, 56] [57] [58] [59] [39]
Cholangiocarcinoma	• Oxidative stress	• Activation of invasion and metastasis through regulation of EMT-associated proteins expression • Enhancement of chronic inflammation response to the tumor microenvironment • Correlation with tumor size, TNM stage, post-operative recurrence, and poor prognosis	[60] [60] [61]
Pancreatic cancer	/	• Inhibition of apoptosis through inhibition of caspase 3 cleavage	[62]
Renal cell carcinoma	/	• Promotion of migration and invasion	[63]
Bladder cancer	• TGF-β	• Increase of cell proliferation • Increase of blood vessel density • Activation of invasion and metastasis through epigenetic silencing of EMT-associated proteins • Induction of epithelial-to-mesenchymal transition	[64] [65] [66] [39]
Colorectal cancer	/	• Increase of cell proliferation through enhanced cell cycle progression • Inhibition of growth suppressors expression • Enhancing of tumor migration and invasion	[67] [68] [69]
Cervical cancer	/	• Inhibition of apoptosis	[70]
Ovarian cancer	• Cisplatin resistance	• Inhibition of pro-apoptotic factors • Activation of invasion and metastasis through regulation of EMT-associated proteins expression • Induction of cisplatin resistance through regulation of cell metabolism	[71] [39] [72]
Leukemia	• Bcr-Abl kinase • c-Myc • ATRA treatment	• Enhancement of drug resistance • Modulation of telomerase activity	[73] [74]
Osteosarcoma	/	• Promotion of cell migration and invasion	[75]
Melanoma	/	• Promotion of glucose metabolism and cell growth	[76]