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17 YAP played a carcinogenic role in a variety of tumors, including prostate cancer and head and neck squamous cell carcinoma. Previous study illuminated that MST1 was highly expressed in hematopoietic cells, and knockdown of MST1 could cause lymphoma development by inducing chromosomal instability. 13, 14, 16Īs reported, MST1 and YAP in the Hippo signaling pathway are differentially expressed in a variety of tumors, thereby participating in the regulation of multiple tumorigeneses. 13, 16 Then, the activated LATS1/2 further phosphorylates the transcriptional coactivator YAP/TAZ which can be sequestered in the cytoplasm and degraded by ubiquitination, hence obstructing the expression of downstream targeted genes.
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13, 16 When Hippo signaling is inactivated, YAP is in an activated state, entering cell nucleus and integrating with transcription factor TEAD, thus inducing a series of genetic expressions related to cell proliferation when Hippo signaling pathway is activated, MST1/2 phosphorylates MOB1 and LATS1/2 and strengthens their interaction with the assistance of scaffolding protein Sav1, so as to activate the phosphorylated LATS1/2. 13, 16 MST1/2, Sav1, LATS1/2, and MOB1 constitute the core kinase chain of the Hippo signaling pathway of mammals. 13 This pathway involves mammalian sterile 20‐like kinases 1/2 (MST1/2), Sav1, large tumor suppressor 1/2 (LATS1/2), MOB1 (MOBKL1A/MOBKL1B), yes‐associated protein (YAP)/transcriptional coactivator with PDZ‐binding motif (TAZ) and TEAD1‐4. Hippo signaling pathway is originally found inside drosophila, which can exert significant regulatory effect on the size of organs. 13, 14 More and more evidences show that Hippo signaling pathway is involved in the oncogenesis of a variety of tumors, such as carcinomas of the lung, pancreas, esophagus, liver, and mammary gland (reviewed in Pan 15). Recently, the Hippo signaling pathway has been reported to promote cell death and differentiation and inhibit cell proliferation. 10, 11 The mutation rates of JAK3 in different studies are greatly varied with a relatively low level, so studies of large samples on its pathogenic mechanism are yet to be conducted for verification. However, some studies on cases of extranodal NKTCL failed to detect any JAK3 genetic mutation.
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In 2014, Bouchekioua et al 9 conducted Sanger sequencing on 24 exons of JAK3, and confirmed three cases of 19 patients suffered JAK3 A573V mutation and one suffered JAK3 V722L mutation. JAK‐STAT signaling pathway also plays an important role in the pathogenic mechanism of extranodal NKTCL and it shows potential value of targeted therapy. 8 These data proved that the continuous activation of the NF‐κB signaling pathway indicated potential carcinogenesis. 7 Studies showed that NF‐κB was up‐regulated in the primary tumor cells of extranodal NKTCL caused by DDX3X (ATP‐dependent RNA helicase) mutation. NF‐κB signaling pathway is extensively involved in the regulation of cell proliferation and development of multiple immune cells. Currently, there are studies showing that the oncogenesis of extranodal NKTCL is closely related to signaling pathways such as NF‐κB, JAK‐STAT, platelet derived growth factor (PDGF), and NOTCH‐1, among which, NF‐κB and JAK/STAT are the best studied in NKTCL. Signaling pathways that regulate the signals of cell growth and development usually play an important role in tumorigenesis and tumor progression. However, given the high malignancy grade, rapid clinical progression and poor long‐term prognosis of extranodal NKTCL, exploring the underlying mechanism of NKTCL is of great significance for the development of drugs for NKTCL. Lin et al 5 and Michot et al 6 increased the 2‐year survival rate of extranodal NKTCL patients to 80.1% and 72% by employing radiotherapy and chemotherapy. 4 Nowadays, it is more common to employ regimens that incorporate radiotherapy and chemotherapy. 3 CHOP (cyclophosphamide, hydroxydaunorubicin, oncovin, prednisone) is a frequently used chemotherapy regimen for NKTCL, but the effect is far from satisfactory.
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2 NKTCL has a unique epidemiological distribution and commonly occurred in East Asia and Latin America. Natural Killer T–Cell Lymphoma (NKTCL) is a subtype of NHL of which the morbidity is ranked the first of T‐Cell Lymphoma. 1 ML can be classified into Hodgkin's Disease (HD) and Non‐Hodgkin's Lymphoma (NHL) according to the histology and pathological pattern. Malignant lymphoma (ML) is a type of malignant tumor that stems from lymph gland and/or extranodal lymphoid tissue, and its morbidity is showing a trend of continuous growth worldwide, becoming a disease that severely impairs human health.