These data suggested that TP73-AS1 served as an oncogene in LAD partially through activating PI3K/AKT pathway and it could be a potential target for diagnosis and treatment of LAD.
Jointly, our findings unveiled that TTN-AS1 plays a carcinogenic part in LAD progression through destabilizing PTEN protein so as to activate PI3K/AKT pathway, therefore indicating TTN-AS1 as a promising target for LAD treatment.
These results provide new evidence for the mechanisms governing the microRNA (miRNA)-ATG12 network and their possible contribution to autophagy modulation and LAD chemoresistance.
Then, using BIRC5 as a candidate, the prognostic value in LAD and TN adenocarcinomas was verified by the Kaplan-Meier plotter and The Cancer Genome Atlas (TCGA) database, respectively.
Overall, the present study demonstrated, for the first time, that the SNHG5/<i>miR-377</i>/CASP1 axis functions as an important role in LAD cells gefitinib resistance and potentially contributes to the improvement of LAD diagnosis and therapy.
Our findings clearly demonstrate that both BP and LAD patients have a dual IgA and IgG autoimmune response to BP180 which is directed not only to the ectodomain, but also to the intracellular portion of this protein.
Clinically, patients with LAD II suffer not only from a less severe form of infectious episodes resembling the moderate phenotype of LAD I but also from severe psychomotor and growth retardation.
Leukocyte adhesion deficiency type-1(LAD-1) is one of the immunodeficiency autosomal recessive diseases that results from mutation in integrin, beta 2 (complement component 3 receptor 3 and 4 subunit) ITGB2 gene.
Leukocyte adhesion deficiency type 1 (LAD 1 - CD18 deficiency) is a rare disease characterized by disturbance of phagocyte function associated with less severe cellular and humoral dysfunction.
LAD I and variant LAD I syndromes are caused by mutations that impair expression or function of integrins of the beta 2 class (CD11/CD18 integrins, or "leukocyte" integrins).
According to the International Multidisciplinary Classification of Lung Adenocarcinoma (LAD) by International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society (IASLC/ATS/ERS) in 2011, the diagnosis of LAD is changing from simple morphology into a comprehensive multidisciplinary classification.
Gain- and loss-of-function tests revealed that CRNDE could influence the radiosensitivity of LAD cells by affecting the G1/S transition and causing apoptosis of LAD cells in vitro.
Mechanistically, LINC00673-v4 augmented the interaction between DDX3 and CK1ε and thus the phosphorylation of dishevelled, which subsequently activated WNT/β-catenin signaling and consequently caused aggressiveness of LAD.