Metabolic reprogramming， as one of the core hallmarks of malignant tumors， plays a key role in the occurrence， development and treatment of breast cancer （BC）. Abnormal changes in glucose metabolism， amino acid metabolism， lipid metabolism， as well as the tricarboxylic acid （TCA） cycle and oxidative phosphorylation （OXPHOS） pathways significantly influence the pathogenesis and progression of BC. Studies have shown that various active components of traditional Chinese medicine （TCM） （such as berberine， matrine， quercetin， curcumin， etc.） and their compound formulations （e.g. Xihuang pill， Danzhi xiaoyao powder， Yanghe decoction， etc.） can inhibit the proliferation and migration of BC cells and induce apoptosis by regulating key metabolic pathways such as glycolysis， lipid synthesis， and amino acid metabolism. TCM demonstrates multi-target and holistic regulatory advantages in intervening in BC metabolic reprogramming， showing significant potential in modulating key molecules like hypoxia inducible factor-1α， hexokinase-2， pyruvate kinase M2， lactate dehydrogenase A， glucose transporter-1， fatty acid synthase， and signaling pathways such as AKT/mTOR. However， current researches still focus predominantly on glucose metabolism， with insufficient mechanistic studies on lipid metabolism， amino acid metabolism， the TCA cycle， and OXPHOS. The precise targets， molecular mechanisms， and clinical translation value of these interventions require further validation and clarification through more high-quality experimental studies and clinical trials.

Objective To investigate the role of STK4-AS1 in regulating the proliferation,invasion,and migration of esophageal squamous cell carcinoma(ESCC)cells through the MYG1/Notch signaling pathway.Methods Quantitative real-time PCR(qRT-PCR)was used to detect the expression of STK4-AS1 in ESCC cells.MTS assay,wound healing and Transwell assay were conducted to explore the proliferation,migration,and invasion abilities in each group in Eca109 and Kyse150 cells.mRNA sequencing(mRNA-seq)was used to detect the down-stream target genes of STK4-AS1.KEGG functional enrichment analyses were used to predict the possible biological processes and signaling pathways.qRT-PCR and western blot were performed to identify mRNA expression of MYG1 and the key downstream transcription factors HES1,HES5,and HEY1 of the Notch signaling pathway,as well as the protein expression of NICD1.Co-transfection plasmids(for over-expressing STK4-AS1 and MYG1)were used to detect the mRNA expression of HES1,HES5,and HEY1 and the protein expression of NICD1 which acted as the key downstream transcription factors in the Notch signaling pathway,as well as the effects on the proliferation,migration,and invasion abilities of ESCC cells.Results The expression of STK4-AS1 was decreased in ESCC cell lines(P<0.01).Over-expression of STK4-AS1 inhibited the proliferation,migration and invasion abilities in Eca109 and Kyse150 cells(P<0.05).STK4-AS1 negatively regulated the expression of MYG1(P<0.01),and the expression of MYG1 was increased in ESCC cell lines(P<0.01).Over-expression of MYG1 could partially reverse the effect of STK4-AS1 on the malignant biological behavior of Eca109 and Kyse150 cells(P<0.05),as well as the mRNA expressions of HES1,HES5,and HEY1 and the protein expression of NICD1(P<0.05).Conclusion STK4-AS1 affects the malignant biological behaviors of ESCC through the MYG1/Notch signaling pathway.

Lung cancer is the malignant tumor with the highest incidence and mortality rates globally. Current treatment methods for lung cancer primarily include surgery， chemotherapy， targeted therapy， and immunotherapy. However， the main limitations of these treatments are their side effects， the drug resistance， and the economic burden they impose. As a critical cancer pathway， the Janus kinase （JAK）/signal transducer and activator of transcription （STAT） signaling pathway regulates tumor occurrence and development through multiple mechanisms by influencing various downstream targets. Consequently， the JAK/STAT signaling pathway offers a promising avenue for lung cancer treatment research. Numerous studies have demonstrated that the JAK/STAT signaling pathway plays a key role in the proliferation and growth of lung cancer cells， angiogenesis， epithelial-mesenchymal transition （EMT）， metabolic alterations， remodeling of the immune microenvironment， and the development of treatment resistance. Traditional Chinese medicine （TCM） has garnered increasing attention due to its minimal side effects， low economic burden， and its potential to enhance efficacy and reduce toxicity when used in conjunction with Western medicine. In addition to traditional Chinese medicine compounds， a growing number of Chinese medicine monomers have come into the spotlight because of their more targeted effects. Numerous studies investigating the regulation of the JAK/STAT signaling pathway by TCM in the treatment of lung cancer have demonstrated that TCM can inhibit the proliferation and invasion of lung cancer cells， tumor angiogenesis， and EMT， improve the inflammatory and immunosuppressive microenvironments， and enhance treatment sensitivity by intervening in the JAK/STAT signaling pathway， thereby impeding the progression of lung cancer. In recent years， the research on the regulation of this pathway by TCM in the treatment of lung cancer has been updated rapidly. However， the summary of these studies has not been updated in time. This review summarizes and reflects on the recent research findings regarding the regulation of the JAK/STAT signaling pathway by TCM to intervene in lung cancer from three aspects， introducing the JAK/STAT pathway， elaborating the mechanism of this pathway in lung cancer， and exploring the intervention of TCM in the treatment of lung cancer through this pathway， to provide more reference for the treatment of lung cancer in the future.

Objective To investigate the role of STK4-AS1 in regulating the proliferation,invasion,and migration of esophageal squamous cell carcinoma(ESCC)cells through the MYG1/Notch signaling pathway.Methods Quantitative real-time PCR(qRT-PCR)was used to detect the expression of STK4-AS1 in ESCC cells.MTS assay,wound healing and Transwell assay were conducted to explore the proliferation,migration,and invasion abilities in each group in Eca109 and Kyse150 cells.mRNA sequencing(mRNA-seq)was used to detect the down-stream target genes of STK4-AS1.KEGG functional enrichment analyses were used to predict the possible biological processes and signaling pathways.qRT-PCR and western blot were performed to identify mRNA expression of MYG1 and the key downstream transcription factors HES1,HES5,and HEY1 of the Notch signaling pathway,as well as the protein expression of NICD1.Co-transfection plasmids(for over-expressing STK4-AS1 and MYG1)were used to detect the mRNA expression of HES1,HES5,and HEY1 and the protein expression of NICD1 which acted as the key downstream transcription factors in the Notch signaling pathway,as well as the effects on the proliferation,migration,and invasion abilities of ESCC cells.Results The expression of STK4-AS1 was decreased in ESCC cell lines(P<0.01).Over-expression of STK4-AS1 inhibited the proliferation,migration and invasion abilities in Eca109 and Kyse150 cells(P<0.05).STK4-AS1 negatively regulated the expression of MYG1(P<0.01),and the expression of MYG1 was increased in ESCC cell lines(P<0.01).Over-expression of MYG1 could partially reverse the effect of STK4-AS1 on the malignant biological behavior of Eca109 and Kyse150 cells(P<0.05),as well as the mRNA expressions of HES1,HES5,and HEY1 and the protein expression of NICD1(P<0.05).Conclusion STK4-AS1 affects the malignant biological behaviors of ESCC through the MYG1/Notch signaling pathway.

OBJECTIVEwe aimed to investigate the mutation and expression of BRAF gene in mature T/NK cell lymphoma tissues and cell lines, explore the correlation between gene alterations and clinicopathological features and clinical outcomes of mature T/NK cell lymphoma.

METHODSFirstly, we detected common mutant sites of BRAF (locus 1 799 mutation in exon 15 and loci 463, 465 and 468 mutation in exon 11) in lymphoma Jurkat, Hut-78 and YTS cell lines, normal peripheral blood lymphocytes, different types of mature T/NK cell lymphoma and reactive hyperplasia lymph nodes by direct sequencing. Then we measured the expression of BRAF in Jurkat, Hut-78, YTS cells and normal peripheral blood lymphocytes by real time-PCR and Western-blot detection. We also used immunohistochemistry (IHC) to detect the expression of BRAF in mature T/NK cell lymphoma tissues and reactive hyperplasia lymph nodes, and to analyze the correlation between the expression of BRAF and clinocopathological features and clinical outcomes.

RESULTSWe did not find common BRAF mutation in mature T/NK cell lymphoma tissues and cell lines, and the relatively expression of BRAF gene mRNA in normal peripheral blood lymphocytes, YTS, Hut-78 and Jurkat cells were 1.000, 5.207±0.013, 8.412±0.615 and 36.720±1.797, respectively, and protein expressions were 0.051±0.003, 0.102±0.013, 0.113±0.017 and 0.304±0.010, respectively, and the expression of BRAF in peripheral T cell lymphoma Jurkat cells was significantly higher than that of Hut-78, YTS cells and normal lymphocytes (P<0.05). Only 6 of 58 peripheral T cell lymphomas (10.3%) had positive BRAF expression, and were the subgroups of peripheral T cell lymphoma-unspecified type. The statistical data did not show any correlation between positive expression of BRAF and gender, age, clinical stage, location, lactate dehydrogenase in the 21 cases of peripheral T cell lymphoma-unspecified type (P<0.05), but the positive rate of BRAF in the effective treatment group (8.3%) was significantly lower than that of the invalid group (55.6%, P<0.05).

CONCLUSIONThe expression of BRAF gene may become a marker of malignant biological characteristics and clinical therapeutic target of peripheral T cell lymphoma.

Exons ; Humans ; Immunohistochemistry ; Killer Cells, Natural ; Lymphoma, T-Cell, Peripheral ; genetics ; metabolism ; pathology ; Proto-Oncogene Proteins B-raf ; genetics ; metabolism ; Pseudolymphoma ; genetics ; metabolism ; RNA, Messenger ; metabolism