Current Knowledge of Long Non-Coding RNA HOTAIR in Breast Cancer Progression and Its Application

Abstract

Breast cancer is one of the most devastating cancers with high morbidity and mortality in females worldwide. Breast tumorigenesis and further development present great uncertainty and complexity, and efficient therapeutic approaches still lack. Accumulating evidence indicates HOX transcript antisense intergenic RNA (HOTAIR) is dysregulated in cancers and has emerged as a novel hotspot in the field. In breast cancer, aberrant HOTAIR expression is responsible for advanced tumor progression by regulating multifarious signaling pathways. Besides, HOTAIR may act as competitive endogenous RNA to bind to several microRNAs and suppress their expressions, which can subsequently upregulate the levels of targeted downstream messenger RNAs, thereby leading to further cancer progression. In addition, HOTAIR works as a promising biomarker and predictor for breast cancer patients’ diagnosis or outcome prediction. Recently, HOTAIR is potentially considered to be a drug target. Here, we have summarized the induction of HOTAIR in breast cancer and its impacts on cell proliferation, migration, apoptosis, and therapeutic resistance, as well as elucidating the underlying mechanisms. This review aims to provide new insights into investigations between HOTAIR and breast cancer development and inspire new methods for studying the association in depth.

lncHUB2: aggregated and inferred knowledge about human and mouse lncRNAs

“…The next cell line with the highest expression of HOTAIR is G401, an epithelial-like kidney cell derived from an infant rhabdoid tumor. It was reported that HOTAIR is highly expressed in atypical rhabdoid tumors ( 78 ). Overall, lncHUB2 prediction about HOTAIR’s biological functions are supported by literature, as well as producing predictions about additional HOTAIR’s roles in normal physiology and disease.…”

Tumor Progression, Microenvironments, and Therapeutics

“…Tumor malignancy starts from transformation [ 1 , 2 , 3 ], apoptotic suppression [ 4 ] tumor proliferation [ 5 , 6 , 7 ], followed by tumor progression [ 2 , 8 , 9 , 10 ], epithelial–mesenchymal transition (EMT), and tumor/metastasis-initiating stemness [ 6 , 11 , 12 ], with which the tumor microenvironments of primary tumor tissues are closely cross-talked [ 8 ]. Primary tumor cells then enter the bloodstream to become circulating tumor cells (CTCs) and colonize into distant organs to form secondary metastatic tumor tissues [ 4 , 13 , 14 ] that lead to cancer death [ 15 ].…”

“…Furthermore, dysregulated HOX transcript antisense intergenic RNA (HOTAIR) in breast cancer endogenously competes with several microRNAs and subsequently upregulates the levels of targeted downstream messenger RNAs, leading to aberrant signal transductions and further cancer progression. Shi et al have summarized current knowledge for the induction of HOTAIR in breast cancer and its impacts on cell proliferation, migration, apoptosis, therapeutic resistance, and the underlying mechanisms, providing new thoughts for anti-cancer therapeutic strategies against breast cancer [ 10 ]. During progression, the proliferation of tumor cells is promoted and apoptosis, including detached cell death anoikis, is suppressed.…”