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2.
Ann Med ; 54(1): 921-932, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-35382656

RESUMO

BACKGROUND: esophageal cancer is one of the deadliest diseases worldwide. Due to the ineffectual screening methods referring to early diagnosis, most people have lost their chance of radical resection when diagnosed with esophageal cancer. This aim of this study was designed to evaluate the latent values of the stem signatures-associated autoantibodies (AABS) in predicting the early diagnosis, and particularly seeking the precise predictive outcomes with sensitive SOX2. We also studied the potential immunotherapeutic targets and prospective long-term prognosis predicators of esophageal cancer. METHODS: The serum concentrations of selective antibodies were quantitated by enzyme-linked immunosorbent assay (ELISA), and a total of 203 local cases were enrolled. The TCGA databases were used to analyse distinct expression patterns and prognostic values of related genes. The TIMER database was used to explore the signatures of immune cell infiltration in related genes. The TISIDB database was used to analyse the association between related genes and immune regulators. RESULTS: The stem signatures-associated with antibodies of TP53, PGP9.5, SOX2, and CAGE were highly expressed in esophageal cancer and were negatively correlated with the test group, the diagnostic sensitivity of P53, SOX2, PGP9.5 and CAGE reached to 54.3%, 56.5%, 80.4% and 47.8%, respectively, and the specificity reached 77.7%, 93.6%, 76.4% and 86.6%. Especially in stage I esophageal cancer, the diagnostic sensitivity of SOX2 reached 82.4% with a specificity of 85.4%, which demonstrated good value in early diagnosis. CONCLUSIONS: The stem signatures-associated antibodies could be used as an effective indicator in early esophageal cancer diagnosis and could help to precisely predicate survival and prognosis.Key MessagesThe stem signatures-associated immune-antibodies could be used as effective indicators in early diagnosis of esophageal cancer and help to precisely predicate the survival and prognosis.The potential immunotherapeutic targets referring to esophageal cancer are screened and analysed, and the high sensitivity of SOX2 in detecting early esophageal cancer will yield early and effective treatments.


Assuntos
Autoanticorpos , Neoplasias Esofágicas , Fatores de Transcrição SOXB1 , Biomarcadores Tumorais , Neoplasias Esofágicas/diagnóstico , Neoplasias Esofágicas/genética , Humanos , Prognóstico , Estudos Prospectivos
3.
J Exp Clin Cancer Res ; 40(1): 325, 2021 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-34656164

RESUMO

BACKGROUND: The small tyrosine kinase inhibitors (TKIs) subversively altered the lung cancer treatments, but patients will inevitably face the therapy resistance and disease recurrence. We aim to explore the potential roles of non-coding RNAs in sensitizing the TKIs effects. METHODS: Multiple cellular and molecular detections were applied to confirm the mechanistic regulations and intracellular connections. RESULTS: We explored the specific gene features of candidates in association with resistance, and found that m6A controlled the stemness of EMT features through METTL3 and YTHDF2. The miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed TUSC7, both of which contributed to the resistant features. Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells' renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. The Notch signaling functions manipulated the cMYC and DICER inner cytoplasm, and the absence of either cMYC or DICER1 lead to TUSC7 and miR-146a decreasing respectively, formed the closed circle to maintain the balance. CONCLUSION: PC9ER and HCC827ER cells harbored much more stem-like cells, and the resistance could be reversed by Notch signaling inactivation. The intrinsic miR-146 and TUSC7 levels are monitored by m6A effectors, the alternation of either miR-146 or TUSC7 expression could lead to the circling loop to sustain the new homeostasis. Further in clinics, the combined delivery of TKIs and Notch specific inhibitory non-coding RNAs will pave the way for yielding the susceptibility to targeted therapy in lung cancer.


Assuntos
Adenocarcinoma de Pulmão/tratamento farmacológico , Cloridrato de Erlotinib/farmacologia , Neoplasias Pulmonares/tratamento farmacológico , Glicoproteínas de Membrana/metabolismo , Metiltransferases/metabolismo , Proteínas do Tecido Nervoso/metabolismo , RNA Longo não Codificante/metabolismo , Receptores Notch/metabolismo , Animais , Linhagem Celular Tumoral , Feminino , Humanos , Camundongos , Camundongos Nus , RNA Longo não Codificante/genética , Transdução de Sinais/efeitos dos fármacos
4.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-358677

RESUMO

<p><b>OBJECTIVE</b>To observe time points of the expressions of basic fibroblast growth factor (bFGF), growth associated protein-43 (GAP-43) and neurogenesis after cerebral ischemia/reperfusion in rats and explore its possible mechanism of neurogenesis.</p><p><b>METHODS</b>Models of middle cerebral artery occlusion (MCAO) were established in SD rats which were divided into 3 d, 7 d, 14 d and 28 d groups (n = 6). The neurological severity was evaluated by neurological severity scores (NSS) and scores of motor test (SMT). Neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining; The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blot and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively.</p><p><b>RESULTS</b>It showed up neurologic impairment and motor dysfunction after cerebral ischemia/reperfusion in rats at 3 d, the numbers of neuron apoptosis also peaked at 3d, the protein levels of bFGF and GAP-43 were significantly increased in time-dependent manner, peaked at 7 d and then decreased gradually, meanwhile, Brdu and NeuN double fluorescence staining displayed scattered Brdu-and NeuN-positive cells in the boundary zone of the infarction area.</p><p><b>CONCLUSION</b>These results suggest that the upregulation of bFGF and GAP-43 may contribute to the neurogenesis after cerebral ischemia/reperfusion.</p>


Assuntos
Animais , Masculino , Ratos , Isquemia Encefálica , Metabolismo , Fator 2 de Crescimento de Fibroblastos , Metabolismo , Proteína GAP-43 , Metabolismo , Neurogênese , Ratos Sprague-Dawley , Traumatismo por Reperfusão , Metabolismo
5.
Acta Pharmaceutica Sinica ; (12): 1065-1071, 2011.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-233034

RESUMO

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.


Assuntos
Animais , Masculino , Ratos , Apoptose , Isquemia Encefálica , Bromodesoxiuridina , Metabolismo , Fator 2 de Crescimento de Fibroblastos , Metabolismo , Proteína GAP-43 , Metabolismo , Infarto da Artéria Cerebral Média , Neurogênese , Neurônios , Patologia , Fármacos Neuroprotetores , Farmacologia , Compostos Orgânicos , Farmacologia , Distribuição Aleatória , Ratos Sprague-Dawley , Traumatismo por Reperfusão , Metabolismo
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