HIF-1 signaling pathway；NF-kappa B signaling pathway；Protein processing in endoplasmic reticulum；Pathways in cancer；Small cell lung cancer；Prostate cancer；PI3K-Akt signaling pathway；Apoptosis；Focal adhesion； Neurotrophin signaling pathway；Cholinergic synapse；Amyotrophic lateral sclerosis (ALS)；Colorectal cancer；Hepatitis B；Epstein-Barr virus infection； Toxoplasmosis；Tuberculosis

Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met.

Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis

NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced β-catenin (a direct target of miRNA-214) protein expression.

Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214

Hepatitis B；Cell cycle；p53 signaling pathway；PI3K-Akt signaling pathway；Measles；Pathways in cancer； Small cell lung cancer；Non-small cell lung cancer；Viral carcinogenesis；Pancreatic cancer；Glioma；Melanoma；Chronic myeloid leukemia

Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107.

Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway

Mineral absorption

NEAT1 may act as a competing endogenous lncRNA to upregulate EGCG-induced CTR1 by sponging hsa-mir-98-5p in NSCLC.

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

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

Additionally, by using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression.

Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway

In our research, lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation.

The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2

In our research, lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation.

The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2

Transcriptional misregulation in cancer

In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis.

NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548

These results suggested that lncRNA NEAT1, whose expression was collaboratively controlled by HuR and miR-124-3p, could regulate ovarian carcinogenesis and may serve as a potential target for antineoplastic therapies.

HuR-regulated lncRNA NEAT1 stability in tumorigenesis and progression of ovarian cancer

In conclusion, knockdown of NEAT1 increased BTB permeability by binding to miR-181d-5p and then reducing tight junction protein expression by targeting SOX5.

Long non-coding RNA NEAT1 regulates permeability of the blood-tumor barrier via miR-181d-5p-mediated expression changes in ZO-1, occludin, and claudin-5

Wnt signaling pathway； Hedgehog signaling pathway；Hippo signaling pathway；Melanogenesis；HTLV-I infection；Pathways in cancer；Proteoglycans in cancer；Basal cell carcinoma

Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling.

Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis

Transcriptional misregulation in cancer

ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.

The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma