Roles of Oncogenic Long Non-coding RNAs in Cancer Development

Abstract

Long non-coding RNAs (lncRNAs) are classified as RNAs that are longer than 200 nucleotides and cannot be translated into protein. Several studies have demonstrated that lncRNAs are directly or indirectly involved in a variety of biological processes and in the regulation of gene expression. In addition, lncRNAs have important roles in many diseases including cancer. It has been shown that abnormal expression of lncRNAs is observed in several human solid tumors. Several studies have shown that many lncRNAs can function as oncogenes in cancer development through the induction of cell cycle progression, cell proliferation and invasion, anti-apoptosis, and metastasis. Oncogenic lncRNAs have the potential to become promising biomarkers and might be potent prognostic targets in cancer therapy. However, the biological and molecular mechanisms of lncRNA involvement in tumorigenesis have not yet been fully elucidated. This review summarizes studies on the regulatory and functional roles of oncogenic lncRNAs in the development and progression of various types of cancer.

Keywords: breast cancer; colorectal cancer; glioblastoma; long non-coding RNA; non-small cell lung cancer; oncogenes.

Fig. 1

Illustrations for the classification of long non-coding RNAs.

Fig. 2

The long non-coding RNA (lncRNA) functions in the nucleus and the cytoplasm.

Fig. 3

Expression levels of PVT1 in non-small cell lung cancers. Datasets obtained from Oncomine demonstrated that lung adenocarcinomas significantly expressed high levels of PVT1 compared to the normal counterparts. (A) Fold change = 2.232, p = 6.13 × 10⁻⁸ [26]. (B) Fold change = 4.293, p = 1.45 × 10⁻⁵ [27]. PVT1, plasmacytoma variant translocation 1.

Fig. 4

Expression levels of SNHG1 in colorectal cancers. Datasets obtained from Oncomine demonstrated that cecum adenocarcinomas (A) (fold change = 2.697, p = 5.22 × 10⁻¹⁴), rectal adenocarcinomas (B) (fold change = 3.333, p = 1.08 × 10⁻²¹), colon adenocarcinomas (C) (fold change = 2.806, p = 2.31 × 10⁻¹⁹), and colon mucinous adenocarcinomas (D) (fold change = 2.241, p = 1.10 × 10⁻¹⁰) significantly expressed high levels of PVT1 compared to the normal counterparts. SNHG1, small nucleolar RNA host gene 1; PVT1, plasmacytoma variant translocation 1.

Fig. 5

Expression levels of NEAT1 in glioblastomas. Datasets obtained from Oncomine demonstrated that GBM significantly expressed high levels of NEAT1 compared to the normal counterparts. (A) Fold change = 5.286, p = 3.18 × 10⁻¹⁴ [46]. (B) Fold change = 4.887, p = 1.15 × 10⁻¹¹ [47]. NEAT1, nuclear paraspeckle assembly transcript 1; GBM, glioblastomas.

Fig. 6

Expression levels of MALAT1 in breast cancers. Datasets obtained from Oncomine demonstrated that invasive ductal breast carcinomas significantly expressed high levels of MALAT1 compared to the normal counterparts. (A) Fold change = 2.600, p = 2.45 × 10⁻⁶ [53]. (B) Fold change = 2.166, p = 6.14 × 10⁻⁴ [54]. MALAT1, metastasis-associated lung adenocarcinoma transcript 1.