Tight junction；Cell cycle；p53 signaling pathway；Bladder cancer；Non-small cell lung cancer；PI3K-Akt signaling pathway；T cell receptor signaling pathway；Hepatitis B；Melanoma；Glioma；Measles；HTLV-I infection；Pathways in cancer；Small cell lung cancer；Viral carcinogenesis；Pancreatic cancer；Chronic myeloid leukemia

Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression.

miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation

HTLV-I infection；Cell cycle；Hepatitis B；Non-small cell lung cancer；Pathways in cancer；Pancreatic cancer；Glioma；Prostate cancer；Melanoma；Bladder cancer；Chronic myeloid leukemia；Small cell lung cancer

Moreover, the present study elucidated the MALAT1-miR-124-CDK4/E2F1 signaling pathway in breast cancer, which might provide a new approach for tackling breast cancer.

miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation

Pathways in cancer；Focal adhesion；MAPK signaling pathway；ErbB signaling pathway；Prostate cancer；Hepatitis C；Hepatitis B；Chemokine signaling pathway；PI3K-Akt signaling pathway；Dorso-ventral axis formation；Osteoclast differentiation；Chronic myeloid leukemia；Gap junction；Fc epsilon RI signaling pathway；Insulin signaling pathway；Renal cell carcinoma ；Endometrial cancer；Non-small cell lung cancer；Proteoglycans in cancer；Glioma；Estrogen signaling pathway；Viral carcinogenesis；Alcoholism；Jak-STAT signaling pathway；Neurotrophin signaling pathway；Natural killer cell mediated cytotoxicity；GnRH signaling pathway；T cell receptor signaling pathway；B cell receptor signaling pathway；Acute myeloid leukemia

Besides, knockdown of MALAT1 increased the expression of miRNA-124, while ectopic expression of miR-124 decreased MALAT1 expression. In addition, we also verified a direct interaction between miR-124 and 3'UTR of GRB2. MALAT1 can indirectly modulate GRB2 expression via competing miR-124.

MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells

PI3K-Akt signaling pathway；MAPK signaling pathway；ErbB signaling pathway；Alcoholism；Neurotrophin signaling pathway；Viral carcinogenesis；Acute myeloid leukemia；Estrogen signaling pathway；Chemokine signaling pathway；GnRH signaling pathway；Endometrial cancer；Prostate cancer；Dorso-ventral axis formation； Glioma；Non-small cell lung cancer；Chronic myeloid leukemia；Pathways in cancer；Proteoglycans in cancer；Osteoclast differentiation；Focal adhesion；Hepatitis B；Gap junction；Jak-STAT signaling pathway；Natural killer cell mediated cytotoxicity；Fc epsilon RI signaling pathway；B cell receptor signaling pathway；Hepatitis C； T cell receptor signaling pathway；Insulin signaling pathway；Renal cell carcinoma

In addition, we also verified a direct interaction between miR-124 and 3'UTR of GRB2. MALAT1 can indirectly modulate GRB2 expression via competing miR-124.

MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells

Notch signaling pathway

In the present study, lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation

Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1