Cholinergic synapse；HIF-1 signaling pathway；Chemokine signaling pathway；MAPK signaling pathway；Small cell lung cancer；Toll-like receptor signaling pathway；Fc epsilon RI signaling pathway；T cell receptor signaling pathway；ErbB signaling pathway；Carbohydrate digestion and absorption；Chagas disease (American trypanosomiasis)；mTOR signaling pathway；PI3K-Akt signaling pathway；Hepatitis B；HTLV-I infection；Pathways in cancer；Toxoplasmosis；Colorectal cancer；Endometrial cancer；Jak-STAT signaling pathway；Neurotrophin signaling pathway；Influenza A；Proteoglycans in cancer； Measles；Dopaminergic synapse；Tuberculosis；Prostate cancer；Non-small cell lung cancer；Apoptosis；Progesterone-mediated oocyte maturation；Melanoma；Chronic myeloid leukemia； B cell receptor signaling pathway； Insulin signaling pathway；Renal cell carcinoma；Estrogen signaling pathway；VEGF signaling pathway；Osteoclast differentiation；Glioma；Epstein-Barr virus infection； Focal adhesion；Tight junction；Hepatitis C；Fc gamma R-mediated phagocytosis；Pancreatic cancer；Acute myeloid leukemia；Adipocytokine signaling pathway

MALAT1 silencing significantly downregulated the expression of the miR-22-3p target gene CXCR2 via reversing the effect of the miR-22-3p, resulting in the aggravation of Oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury； this process was associated with the AKT pathway.

The lncRNA MALAT1 protects the endothelium against ox-LDL-induced dysfunction via upregulating the expression of the miR-22-3p target genes CXCR2 and AKT

We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.

Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206

Regulation of autophagy

Furthermore, MALAT1 may serve as a molecular sponge for miR-30a and negatively regulate its expression. In addition, MALAT1 overturned the inhibitory effect of miR-30a on ischemic injury and autophagy in vitro and in vivo, which might be involved in the derepression of Beclin1, a direct target of miR-30a.

Down-Regulation of Lncrna MALAT1 Attenuates Neuronal Cell Death Through Suppressing Beclin1-Dependent Autophagy by Regulating Mir-30a in Cerebral Ischemic Stroke.

Legionellosis

In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.

Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury

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

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

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Epithelial cell signaling in Helicobacter pylori infection

MALAT1 silencing significantly downregulated the expression of the miR-22-3p target gene CXCR2 via reversing the effect of the miR-22-3p, resulting in the aggravation of Oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury； this process was associated with the AKT pathway.

The lncRNA MALAT1 protects the endothelium against ox-LDL-induced dysfunction via upregulating the expression of the miR-22-3p target genes CXCR2 and AKT

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Axon guidance；Leukocyte transendothelial migration；Intestinal immune network for IgA production

By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion. Taken together, our data indicated that MALAT1 might play an oncogenic role in HCCA through miR-204-dependent CXCR4 regulation, and could be regarded as a therapeutic target in HCCA.

Long Non-Coding RNA MALAT1 Interacted with miR-204 to Modulates Human Hilar Cholangiocarcinoma Proliferation, Migration and Invasion by Targeting CXCR4

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Axon guidance；Leukocyte transendothelial migration；Intestinal immune network for IgA production

Knockdown of MALAT1 inhibited the proliferation, migration, and invasion of human HCCA cell. In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration, and invasion. By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion.

Long Non-Coding RNA MALAT1 Interacted with miR-204 to Modulates Human Hilar Cholangiocarcinoma Proliferation, Migration and Invasion by Targeting CXCR4

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

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

Moreover, luciferase assays showed that miR-23c, as a target of MALAT1, directly repressed ELAVL1 expression and then decreased the expression of its downstream protein NLRP3.

Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy

EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin. Furthermore, targeted inhibition of MALAT1 or EZH2 reversed EMT and chemoresistance induced by oxaliplatin. Finally, the interaction between lncRNA MALAT1 and miR-218 was observed, which further indicated its prognostic value in patients who received standard FOLFOX (oxaliplatin combine with 5-fluorouracil and leucovorin) treatment.

MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2

Ubiquitin mediated proteolysis

Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.

Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function

Hedgehog signaling pathway；Hippo signaling pathway；Pathways in cancer；Basal cell carcinoma

Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202.

Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression

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

Pathways in cancer；Renal cell carcinoma

It was HIF-2α, but not HIF-1α induced MALAT1 upregulation in HCC cells. Dual luciferase assay demonstrated that there were at least two binding sites of miR-26b in MALAT1.

The HIF-2α-MALAT1-miR-216b axis regulates multi-drug resistance of hepatocellular carcinoma cells via modulating autophagy

Base excision repair

Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis.

MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p

Base excision repair

Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis.

MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p

Adherens junction；HIF-1 signaling pathway；Oocyte meiosis；Endocytosis；PI3K-Akt signaling pathway；Focal adhesion；Prostate cancer；Long-term depression；Ovarian steroidogenesis；Proteoglycans in cancer；Glioma；Progesterone-mediated oocyte maturation；Pathways in cancer；Melanoma；Transcriptional misregulation in cancer

Furthermore, the miR-122-IGF-1R signaling correlated with the dysregulated MALAT1 expression in gastric cancer.

The lncRNA MALAT1 is a novel biomarker for gastric cancer metastasis

Axon guidance；Phagosome；PI3K-Akt signaling pathway；Focal adhesion；ECM-receptor interaction；Toxoplasmosis；Cell adhesion molecules (CAMs)；Leukocyte transendothelial migration；Regulation of actin cytoskeleton；Hypertrophic cardiomyopathy (HCM)；Dilated cardiomyopathy；Proteoglycans in cancer；Arrhythmogenic right ventricular cardiomyopathy (ARVC)；Bacterial invasion of epithelial cells；Leishmaniasis；Pathogenic Escherichia coli infection；Pertussis；Pathways in cancer；Small cell lung cancer；Shigellosis

We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin β1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1.

Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation

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

KDM5B-silencing in the TNBC cells correlated with the upregulation of hsa-miR-448 and led to suppression of MALAT1 expression with decreased migration, invasion and clonogenic capacity in vitro, as well as, poor survival in vivo.

Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448

Natural killer cell mediated cytotoxicity；MAPK signaling pathway；ErbB signaling pathway；Chemokine signaling pathway；PI3K-Akt signaling pathway；Insulin signaling pathway；Hepatitis C；Long-term potentiation；Progesterone-mediated oocyte maturation；Dorso-ventral axis formation；Axon guidance；Endometrial cancer；Regulation of actin cytoskeleton；VEGF signaling pathway；Long-term depression；Estrogen signaling pathway；Cholinergic synapse；Melanogenesis；Hepatitis B；Viral carcinogenesis；Tight junction；Neurotrophin signaling pathway；GnRH signaling pathway；Gap junction；Glioma；T cell receptor signaling pathway； Alcoholism；Prostate cancer；Serotonergic synapse；Bladder cancer；Non-small cell lung cancer；Chronic myeloid leukemia；HTLV-I infection；B cell receptor signaling pathway；Pathways in cancer；Aldosterone-regulated sodium reabsorption；Colorectal cancer；Melanoma；Acute myeloid leukemia；Proteoglycans in cancer；Pancreatic cancer；Renal cell carcinoma；Thyroid cancer；Fc epsilon RI signaling pathway

We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.

Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206

PI3K-Akt signaling pathway

Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells.

The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer

GnRH signaling pathway

We determined that MALAT1 promotes melanoma cells proliferation, invasion and migration by sponging miR-22. MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.

Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22

Axon guidance；MAPK signaling pathway；Chemokine signaling pathway；Natural killer cell mediated cytotoxicity；Fc epsilon RI signaling pathway；B cell receptor signaling pathway；Phagosome；PI3K-Akt signaling pathway；Pancreatic cancer；Wnt signaling pathway；Leukocyte transendothelial migration；Amyotrophic lateral sclerosis (ALS)；VEGF signaling pathway；Regulation of actin cytoskeleton；Proteoglycans in cancer；Epithelial cell signaling in Helicobacter pylori infection；Osteoclast differentiation；Shigellosis；Focal adhesion；Adherens junction；Neurotrophin signaling pathway；Salmonella infection；Renal cell carcinoma；Viral myocarditis；Pancreatic secretion；Pathways in cancer；Colorectal cancer；Toll-like receptor signaling pathway；Fc gamma R-mediated phagocytosis；Bacterial invasion of epithelial cells；Viral carcinogenesis

Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs.

MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis

Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells.

RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal 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

Hippo signaling pathway；Adherens junction

In particular, MALAT1 upregulated the expression of miR-204 target gene SLUG through competitively 'spongeing' miR-204.

LncRNA MALAT1 exerts oncogenic functions in lung adenocarcinoma by targeting miR-204

Pancreatic cancer；Cell cycle；Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer；Colorectal cancer；Chronic myeloid leukemia

In vitro experiments revealed that MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers, including alkaline phosphatase, mineralized bone matrix formation and osteocalcin. Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1. Thus, MALAT1 positively regulated the expression of Smad4 through sponging miR-204, and promoted osteogenic differentiation of VICs.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.

Cell cycle； Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer； Colorectal cancer；Pancreatic cancer；Chronic myeloid leukemia

Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.

Hippo signaling pathway；MAPK signaling pathway；Cytokine-cytokine receptor interaction；Cell cycle；Endocytosis；TGF-beta signaling pathway；Renal cell carcinoma；Hypertrophic cardiomyopathy (HCM)；Chronic myeloid leukemia；Toxoplasmosis；Pathways in cancer；Osteoclast differentiation；HTLV-I infection；Proteoglycans in cancer；Intestinal immune network for IgA production；Rheumatoid arthritis；Dilated cardiomyopathy；Hepatitis B；Pancreatic cancer；Leishmaniasis；Tuberculosis；Chagas disease (American trypanosomiasis)；Colorectal cancer； Malaria

MALAT1 and miR-200c are reciprocally repressed, and TGF-β increased MALAT1 expression by inhibiting miR-200c.

Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma

NF-kappa B signaling pathway；MAPK signaling pathway；Ubiquitin mediated proteolysis；Endocytosis；Chagas disease (American trypanosomiasis)；Osteoclast differentiation；Toll-like receptor signaling pathway；Herpes simplex infection；NOD-like receptor signaling pathway；Hepatitis C；RIG-I-like receptor signaling pathway；Neurotrophin signaling pathway； Toxoplasmosis；Measles；Pertussis；Leishmaniasis；Tuberculosis；Small cell lung cancer；Epstein-Barr virus infection；Pathways in cancer

Remarkably, TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6. Furthermore, we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b-5p to down-regulate its expression in HCC.

Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis

Endocytosis；MAPK signaling pathway；NF-kappa B signaling pathway；Ubiquitin mediated proteolysis；Osteoclast differentiation；Chagas disease (American trypanosomiasis)；Small cell lung cancer；Measles； Toxoplasmosis；Tuberculosis；Toll-like receptor signaling pathway；Pathways in cancer；NOD-like receptor signaling pathway；RIG-I-like receptor signaling pathway；Neurotrophin signaling pathway； Hepatitis C；Pertussis；Epstein-Barr virus infection；Leishmaniasis；Herpes simplex infection

Remarkably, TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6. Furthermore, we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b-5p to down-regulate its expression in HCC.

Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis.

Pyrimidine metabolism；One carbon pool by folate；Metabolic pathways

LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression.

MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression

We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC.

LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma

We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC.

LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma

We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC.

LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma

Adherens junction；Tight junction；Gap junction；Vibrio cholerae infection；Epithelial cell signaling in Helicobacter pylori infection；Salmonella infection

Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted.

Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140