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Table 3. Summary of key targets, potential pathogenesis mechanisms, and treatment significance in NKTCL epigenetic variations
The alterations Potential Role in pathogenic mechanism of Potential treatment
of human hallmark/signaling lymphoma Ref. significance Ref.
genetics pathways
Epigenetic PTPRK Downregulated for methylation or Chen et al. [48] PTPRK may be a potential N/A
variations deletion and mediates inhibition of cells target of NKTCL
proliferation, invasion, and migration epigenetic therapy
[63]
HACE1 Encodes E3 ubiquitin ligase and inhibits Zhang et al. N/A N/A
cell cycle progression, but silenced due
to CpG methylation
The specific function of HACE1 is not
clear
[67]
TET1 Frequently methylated, and the Li et al. N/A N/A
oncogenic mechanism has not been
revealed
KMT2D Mutations may cause dysregulation of Choi et al. [43] N/A N/A
gene transcription regulation
BCOR Loss of function mutations of BCOR are Dobashi et al. [41] N/A N/A
considered highly specific in NKTCL

NKTCL: Extranodal natural killer/T cell lymphoma; PTPRK: receptor-type tyrosine-protein phosphatase κ; HACE1: HECT domain and ankyrin
repeat containing E3 ubiquitin-protein ligase 1; CpG: cytosine-phosphate-guanine; TET1: methylcytosine dioxygenase ten-eleven translocation 1;
KMT2D: lysine [K]-specific methyltransferase 2D; BCOR: bcl6 corepressor.

Table 4. Important non-coding RNAs and their potential roles and therapeutic significance associated with NKTCL
The alterations Potential Role in pathogenic Potential treatment
of human hallmark/signaling mechanism of lymphoma Ref. significance Ref.
genetics pathways
microRNAs miR-15a Downregulated in NKTCL cell Komabayashi May predict poor response to Komabayashi
lines et al. [71] treatment and survival of et al. [71]
NKTCL patients
miR-21 Upregulated and mediates Yamanaka N/A N/A
apoptotic activity reduction et al. [74]
[72]
miR-146a Overexpressed and may limit Paik et al. N/A N/A
Bcl-2 expression by inhibiting
NF-κB pathway
[69] [70]
miR-150 Downregulated in NKTCL Ng et al. Overexpression of miR-150 Wu et al.
tumor tissues and in vitro impacts the sensitivity to
radiotherapy
miR-155 Overexpressed and induce Yamanaka N/A N/A
[74]
aberrant activation of et al.
SHIP1/AKT pathway
[73]
miR-223 Upregulated and targets and Liang et al. N/A N/A
downregulates PRDM1
[76] [76]
lncRNAs BCYRN1 Upregulated and may induce Wang et al. Aberrant expression of Wang et al.
autophagy BCYRN1 enhances resistance
to L-asparaginase.
[77]
XIST Overexpressed and mediates Liu et al. N/A N/A
proliferation and migration in
vitro
SNHG12 Upregulated and advances Zhu et al. [78] C-myc may suppress the Zhu et al. [78]
cell proliferation as a direct response to cisplatin by
transcription target of c-myc promoting SNHG12 expression
in NKTCL
NKTCL: Extranodal natural killer/T cell lymphoma; Bcl-2: B cell leukemia/lymphoma 2; NK-κB: nuclear factor kappaB; SHIP1/AKT: inositol
polyphosphate-5-phosphatase D/ protein kinase B; PRDM1: PR/SET domain 1; BCYRN1: brain cytoplasmic RNA 1; XIST: X-inactive-specific
transcript; SNHG12: small nucleolar RNA host gene 12.

cells and inhibits the activation, proliferation, and cytokine expression of T cells . The combination of PD-
[79]