Like protein-coding genes and miRNAs, lncRNAs can function as oncogenes or tumor suppressors during cancer progression. A further investigation of the roles and mechanisms of lncRNAs in cancer will provide novel lncRNA-based strategies for the treatment of human cancers. Some well-studied lncRNAs, such as HOTAIR [
16,
48], MALAT1 [
52], PCAT-1 [
27], PCGEM1 [
55], TUC338 [
56], were reported as oncogenes, while GAS5 [
63], linc-p21 [
29], MEG3 [
64] and PTENP1 [
40] were reported as tumor suppressors. Here, we mainly focus on recently studied lncRNAs.
The newly identified lncRNA BANCR was found overexpressed in melanoma and required for full migratory capacity of melanoma cells by upregulating CXCL11, an important gene involved in cell migration, revealing the potential functional role of lncRNA BANCR [
57]. Another novel lncRNA YIYA is upregulated in different cancers and promotes cell cycle progression at the G1/S transition, demonstrating it is a carcinogenesis-associated lncRNA [
58]. A recent study found that lncRNA CRNDE is highly elevated in many solid tumors and in acute myeloid leukemias (AML), especially in M2 AML and M3 AML, and lncRNA CRNDE can promote cell growth and suppress apoptosis, which supports a role for CRNDE as a mediator of oncogenesis [
59]. More recently, it was reported that lncRNA CCAT1, activated by c-Myc, is markedly increased in gastric carcinoma and promote cell proliferation and migration, implicating CCAT1 as a potential therapeutic target [
60]. Studies also showed that induction of lncRNA HULC by Hepatitis B virus X protein (HBx) promotes proliferation of hepatoma cells through downregulating tumor suppressor gene p18
in vitro and
in vivo[
61]. In addition, it was found that lncRNA CUDR, a variant transcript of lncRNA UCA1, is upregulated in various human tumors and can significantly enhance proliferation, migration and invasion of the bladder cancer cell
in vitro and
in vivo, indicating lncRNA CUDR functions as an oncogene and may serve as a novel therapeutic target for bladder cancer [
62]. Compared with these oncogenic lncRNAs, some lncRNAs showed a tumor suppressive role. The lncRNA MEG3 (maternally expressed gene 3), which is associated with meningioma pathogenesis and progression [
64], was recently found markedly decreased in glioma tissues and ectopic expression of lncRNA MEG3 inhibited cell proliferation and promoted cell apoptosis via p53 activation in human glioma [
65]. Very interestingly, a study reported that lncRNA PTCSC3 (Papillary Thyroid Carcinoma Susceptibility Candidate 3), located 3.2 kb downstream of SNP rs944289 at 14q.13.3, is strongly downregulated in papillary thyroid carcinoma (PTC). The overexpression of lncRNA PTCSC3 could inhibit PTC cell growth and affected the expression of genes involved in DNA replication, recombination and repair, cellular movement, tumor morphology, and cell death, implying that lncRNA PTCSC3 has the characteristics of a tumor suppressor [
68]. Further study revealed that SNP rs944289 abolishes the binding site of both C/EBPα and C/EBPβ, which bind and activate the PTCSC3 promoter, thus, SNP rs944289 predisposes to PTC through downregulating tumor suppressive lncRNA PTCSC3 [
68].