miRNA
Regulation periodontally affected tissues
Type of immune system affected in periodontitis
Mechanism
Upregulated
Downregulated
miR-30e
–
Yes
Innate immune system
Inhibits NK cell activation. This downregulation increases NK cell activation and hence increases tissue destruction
miR-31
–
Yes
Innate immune system
Negative regulator of NF-κB and mediates osteoclastogenesis. Its downregulation produces over-activation of TLRs and decreases bone formation
miR-146a
Yes
–
Innate and adaptive immune system
Regulates NF-κB signaling pathway activation, reduces dendritic cell cytokine production, impairs dendritic cell TLRs, and controls B-cell development
miR-148a
Yes
–
Innate and adaptive immune system
Impairs antigen presentation function by dendritic cells and the whole innate response
miR-155
Yes
–
Innate and adaptive immune system
Regulates NF-κB signaling pathway, mediates type I interferon and interferon-gamma production; increases TLR sensitivity, critical in dendritic cell maturation; controls CD8 T-cell response; and indirectly influences the activation of T-helper cell 17
miR-200a
–
Yes
Innate immune system
Negative regulation of IL-12 in NK cells. Thus, its downregulation causes increased production
miR-210
–
Yes
Adaptive immune system
Its downregulation increases T-cell signaling
miR-451
Yes
–
Innate immune system
Suppression of neutrophil chemotaxis
miR-486
Yes
–
Innate immune system
Increases exponentially NF-κB signaling pathway
miR-650
Yes
–
Adaptive immune system
Regulates B-cell proliferation
Main lncRNAs in periodontally affected gingival tissues
|
lncRNA |
Regulation periodontally affected tissues |
Type of immune system affected in periodontitis |
Mechanism |
|
|---|---|---|---|---|
|
Upregulated |
Downregulated |
|||
|
HOTAIR |
Yes |
– |
Still unknown |
|
|
RP3-461P17 RP1-300I2.2 |
– |
Yes |
– |
Still unknown |
|
TIRAP |
Yes |
– |
– |
Still unknown |
|
CDKN2A |
Yes |
– |
– |
Still unknown |
|
CDKN2B |
Yes |
– |
– |
Still unknown |
|
lincRNA-CDON-1 |
Yes |
– |
Innate immune system |
Affects signaling pathways of TLR activation |
|
ANRIL |
– |
Yes |
Regulation of chromatin, ADIPOR1, VAMP3, and C11ORF10 expression. Its downregulation provokes reduced expression of those markers, increasing the risk of atherosclerosis, metabolic syndrome, periodontitis, and several forms of cancer |
|
Some examples of methylations in cancer expression
|
Author/year |
Country |
Type of cancer involved |
Epigenetic modification |
Results |
Mechanism |
|
|---|---|---|---|---|---|---|
|
Upregulation of cancer |
Downregulation of cancer |
|||||
|
[94] |
Belgium |
Melanoma |
DNMT1 |
Yes |
Yes |
Transient depletion of DNMT1 can lead to long-term activation of cancer-germline genes and repression of mitosis/division-related genes at the same time |
|
[95] |
USA |
Colon cancer |
DNMT1 |
– |
Yes |
Interaction between a subset of lncRNAs and DNMT1 was reduced in colon cancer cells, which contributes to aberrant DNA methylation and gene expression in tumorigenesis |
|
[96] |
USA |
Lung cancer |
DNMT1 |
Yes |
– |
There is a cross talk between tyrosine-protein kinase KIT and DNMT1 in the development of drug resistance, which implies an upregulation of oncogenesis process by means of that interaction |
|
[97] |
China |
Breast cancer |
DNMT1 |
Yes |
– |
DNMT1, DNMT3A, and DNMT3B commonly or individually contributed to DNA methylation in different breast cancer cells |
Some examples of histone acetylations in cancer expression
|
Author/year |
Country |
Type of cancer involved |
Epigenetic modification |
Results |
Mechanism |
|
|---|---|---|---|---|---|---|
|
Upregulation of cancer |
Downregulation of cancer |
|||||
|
[98] |
China |
Hepatocellular carcinoma |
Histone acetylation |
– |
Yes |
Histone deacetylase (HDAC) 9 increased the expression of miR-376a by upregulating the global histone H3K18 acetylation level, which is inversely correlated with hepatocellular carcinoma |
|
[99] |
Poland |
Colorectal cancer |
Histone acetylation |
Yes |
– |
Histone H3 lysine 27 acetylation (H3K27Ac) is upregulated in CRC |
|
[100] |
Germany |
Lymphoma, hepatoma, |
Histone acetylation |
Yes |
– |
The 5-HTT gene is epigenetically downregulated by histone deacetylation. The 5-HTT gene is usually silenced in several types of cancer |
Some examples of miRNAs and lncRNAs in cancer expression
|
Author/year |
Country |
Type of cancer involved |
Epigenetic modification |
Results |
Mechanism |
|
|---|---|---|---|---|---|---|
|
Upregulation of Cancer |
Downregulation of Cancer |
|||||
|
[90] |
USA |
Pancreatic cancer |
miR-31 |
Yes |
– |
Expression of enforced miR-31 significantly enhanced invasion and migration of multiple pancreatic cancer cells |
|
[89] |
Taiwan |
Oral potentially malignant disorder |
miR-31 |
Yes |
– |
Epithelial dysplasia and miR-31 upregulation synergistically predict the increased incidence of recurrence and/or malignant transformation in patients with OPMD. Detection of miR-31 expression is an adjuvant method for screening of high-risk OPMD |
|
[91] |
Germany |
Head and neck squamous cell carcinoma |
miR-146a and miR-155 |
Yes |
– |
Downregulation of miR-146a and miR-155 in blood of patients correlated with the occurrence of distant metastasis regarding tumor patients |
|
[93] |
China |
Oral squamous cell carcinoma |
Long noncoding RNA-HOX transcript antisense intergenic RNA (HOTAIR) |
Yes |
– |
HOTAIR was highly expressed in OSCC tissues and facilitated the growth of OSCC cells, thus probably being an eligible molecular marker for OSCC diagnosis and prognosis determination |
|
[93] |
Oral squamous cell carcinoma |
Long noncoding RNA-HOX transcript antisense intergenic RNA (HOTAIR) |
Yes |
– |
Overexpression of HOTAIR indicated poor overall survival in OSCC patients. Knockdown of HOTAIR in OSCC cells decreased cell proliferation and colony formation, increased cell invasion and migration, and induced apoptosis in vitro |
|
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