Cysteine and methionine metabolism；Metabolic pathways

Therefore, we infer that miR-375 is downregulated partly due to promoter hypermethylation mediated by DNMT1 in HPV-16 positive cervical cancer cells. Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels

MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1

PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195.

LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells

Mechanistically, we verified that PVT1 binds to EZH2, recruits EZH2 to the miR-200b promoter, increases histone H3K27 trimethylation level on the miR-200b promoter, and inhibits miR-200b expression.

Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b

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

Herpes simplex infection；Endocytosis； Phagosome；Cell adhesion molecules (CAMs)；Antigen processing and presentation；Natural killer cell mediated cytotoxicity；Type I diabetes mellitus；HTLV-I infection；Graft-versus-host disease；Epstein-Barr virus infection； Viral myocarditis；Viral carcinogenesis；Autoimmune thyroid disease；Allograft rejection

Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a.

Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer

Amphetamine addiction

Remarkably, SIRT1 was confirmed as a direct target of miR-138-5p in cervical cancer and miR-138-5p exerted the tumor suppressed functions by suppressing SIRT1 expression.

Decreased Expression of MiR-138-5p by LncRNA H19 in Cervical Cancer Promotes Tumor Proliferation.