Cell cycle；p53 signaling pathway；Endometrial cancer；Melanoma；Thyroid cancer；PI3K-Akt signaling pathway；Pancreatic cancer；Wnt signaling pathway；Hippo signaling pathway；Prostate cancer；Acute myeloid leukemia；Focal adhesion；Viral myocarditis；Viral carcinogenesis；Colorectal cancer；Jak-STAT signaling pathway；Hepatitis B；Measles；Proteoglycans in cancer；Bladder cancer；Non-small cell lung cancer；HTLV-I infection；Small cell lung cancer；Pathways in cancer；Glioma；Chronic myeloid leukemia

Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1.

Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma

Chemokine signaling pathway；MAPK signaling pathway；Endocytosis；Axon guidance；Epithelial cell signaling in Helicobacter pylori infection；Viral carcinogenesis；Neurotrophin signaling pathway；Bacterial invasion of epithelial cells；Renal cell carcinoma；Shigellosis；Salmonella infection；Pancreatic cancer；VEGF signaling pathway；Focal adhesion；Pathways in cancer；Pathogenic Escherichia coli infection；Adherens junction；Tight junction；GnRH signaling pathway；Regulation of actin cytoskeleton；T cell receptor signaling pathway；Fc gamma R-mediated phagocytosis；Leukocyte transendothelial migration；Proteoglycans in cancer

In this study we identified long non-coding RNA (lncRNA) MALAT1 can function as a ceRNA of cell division cycle 42 (cdc42) 3'UTR in inducing migration and invasion of breast cancer cells via miR-1. We found that miR-1 bound both MALAT1 and cdc42 3'UTR directly.

MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42

Taken together, these results suggest that HOTAIR is a FOXC1-activated driver of malignancy, which acts in part through the repression of miR-1.

HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma

Hippo signaling pathway；Adherens junction

In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. We proposed that MALAT1 exerted its function through the miR-1/slug axis.

Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development

Hippo signaling pathway；Adherens junction

Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1.

The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma