Lung cancer is the leading cause of cancer-related deaths worldwide， and tumor metastasis is a key factor contributing to the mortality of most lung cancer patients. Aberrant activation of epithelial-mesenchymal transition （EMT） is a major driver of lung cancer progression and metastasis. EMT is characterized by the loss of apical-basal polarity and intercellular adhesion in highly differentiated， polarized， and organized epithelial cells， which acquire motility， migratory potential， and invasive properties. During this process， cells undergo cytoskeletal remodeling and transform into a mesenchymal phenotype， accompanied by associated changes in cellular markers. The EMT process is highly complex and is tightly regulated by intricate networks involving multiple transcription factors， post-translational controls， epigenetic modifications， and non-coding RNAs. Therefore， therapies targeting the mechanisms of malignant transformation and their associated pathways in lung cancer are of significant clinical importance. In recent years， EMT has attracted increasing attention as a potential target for cancer therapy. Chinese medicine， with its characteristics of multi-target action， low side effects， and good therapeutic efficacy， has demonstrated an important role in anticancer treatment. A series of studies have investigated the role of Chinese medicine in inhibiting EMT in lung cancer. Active ingredients of Chinese medicine， including flavonoids， glycosides， phenols， terpenoids， saccharides， and alkaloids， as well as Chinese medicine compound formulas， have shown significant regulatory effects on EMT. Their mechanisms mainly involve multiple pathways， targets， and links， including signaling pathways， exosomes， microRNAs （miRNAs）， and the tumor-associated immune microenvironment. This article summarizes the mechanisms by which EMT promotes malignant tumor progression and reviews the current research on how Chinese medicine active ingredients， monomers， and compound formulas inhibit EMT and suppress lung cancer cell migration and invasion. This study is expected to provide comprehensive theoretical information for basic and translational research on lung cancer.

Objective To compare the cost and efficacy of ambulatory versus hospitalized surgery for lung tumor patients. Methods Two researchers independently conducted a computer search on February 14, 2025, in databases including CNKI, PubMed, Web of Science, Ovid Medline, Cochrane Library, and Wanfang Database, with the search period covering from the inception of these databases to February 2025. The outcome indicators were postoperative complication rate, length of hospital stay, hospitalization costs, et al. For the included randomized controlled trials and non-randomized controlled trials, we used the Cochrane risk of bias assessment tool and the Newcastle Ottawa Scale (NOS) respectively to evaluate the quality of the literature, and extracted data from the included studies for meta-analysis using RevMan 5.4 and Stata 18.0. Results A total of 12 researches were ultimately included, consisting of 2 randomized controlled trials, 2 prospective cohort studies, and 8 retrospective cohort studies, involving a total of 76 403 patients. All researches were evaluated as high-quality. Meta-analysis showed that the ambulatory surgery group had advantages over the hospitalized surgery group in terms of operation time [MD=−21.07, 95%CI (−30.55, −11.58), P<0.001], length of hospital stay [MD=−2.17, 95%CI (−3.25, −1.09), P<0.001], hospitalization costs [SMD=−1.22, 95%CI (−2.18, −0.26), P=0.01], and overall postoperative complications [OR=0.48, 95%CI (0.32, 0.74), P<0.001]. There was no statistically significant difference between the two groups in terms of postoperative hoarseness [OR=0.62, 95%CI (0.24, 1.61), P=0.33] and postoperative chylothorax [OR=0.27, 95%CI (0.07, 1.07), P=0.06]. Conclusion Compared to conventional hospitalized lung tumor resection, ambulatory lung tumor resection can significantly reduce the patient’s surgery and hospital stay time, decrease hospitalization costs, and reduce the incidence of postoperative complications. Ambulatory surgery can improve hospital efficiency while reducing the economic burden on patients. It is worthy of further promotion and application.

ObjectiveTo evaluate the effects of Tongnaoyin on the blood-brain barrier status and neurological impairment in acute ischemic stroke （AIS） patients with the syndrome of phlegm-stasis blocking collaterals by dynamic contrast-enhanced magnetic resonance imaging （DCE-MRI）. MethodsA total of 63 patients diagnosed with AIS in the Jiangsu Province Hospital of Chinese Medicine from October 2022 to December 2023 were enrolled in this study. According to random number table method，the patients were assigned into a control group （32 cases） and an observation group （31 cases）. The control group received conventional Western medical treatment，and the observation group took 200 mL Tongnaoyin after meals，twice a day from day 2 of admission on the basis of the treatment in the control group. After 7 days of treatment，the patients were examined by DCE-MRI. The baseline data for two groups of patients before treatment were compared. The National Institute of Health Stroke Scale （NIHSS） score and modified Rankin Scale （mRS） score were recorded before treatment and after 90 days of treatment for both groups. The rKtrans，rKep，and rVe values were obtained from the region of interest （ROI） of the infarct zone/mirror area and compared between the two groups. ResultsThere was no significant difference in the NIHSS or mRS score between the two groups before treatment. After 90 days of treatment，the NIHSS and mRS scores declined in both groups，and the observation group had lower scores than the control group （P<0.05）. After treatment，the rKtrans and rVe in the observation group were lower than those in the control group （P<0.01）. ConclusionCompared with conventional Western medical treatment alone，conventional Western medical treatment combined with Tongnaoyin accelerates the repair of the blood-brain barrier in AIS patients，thereby ameliorating neurological impairment after AIS to improve the prognosis.

Tumorigenesis， invasion， and metastasis occur in the context of a persistent inflammatory microenvironment， and a variety of inflammatory factors can lead to the development of various tumors. Guided by the thought of "preventive treatment of disease" in TCM and the concept of tertiary prevention in modern medicine， it is of great significance to effectively intervene in the inflammatory stage of the disease， interrupt disease progression， prevent the occurrence of malignant tumors， and reverse the process of "inflammation-to-cancer transformation". Sinisan， a commonly used prescription in the Treatise on Febrile Diseases， has been widely applied in the treatment of precancerous lesions of the digestive system， demonstrating considerable advantages. This article reviewed literature from the past 20 years， summarizing the application of Sinisan in precancerous lesions of the digestive system from three aspects： the exploration of its prescription-syndrome relationship， clinical application， and mechanistic study. It is found that basic syndrome indications of Sinisan include harmonizing the Earth element to promote spleen-stomach transportation and transformation， soothing the liver and nourishing the Wood element to restore the smooth flow of Qi， and regulating Yin and Yang to relieve stagnation within the system. In clinical application， Sinisan has shown significant efficacy in atrophic gastritis and precancerous conditions such as intestinal metaplasia， gastric ulcer， ulcerative colitis， esophagitis， and pancreatitis. Mechanistic studies have revealed that Sinisan can inhibit inflammatory factors and improve the inflammatory microenvironment， inhibit cell proliferation and regulate apoptosis， exhibit anti-angiogenic and antitumorigenic effects， modulate immune function， and exert antioxidant effects. These mechanisms can be achieved by regulating pathways such as nuclear factor erythroid 2-related factor 2/heme oxygenase-1 （Nrf2/HO-1）， farnesoid X receptor （FXR）/Nrf2， phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt）， Takeda G protein-coupled receptor 5/cyclic adenosine monophosphate/protein kinase A （TGR5/cAMP/PKA）， interleukin-4/signal transducer and activator of transcription 6 （IL-4/STAT6）， Janus kinase/signal transducer and activator of transcription （JAK/STAT）， RhoA/Rho-associated protein kinase （RhoA/ROCK）， and transforming growth factor-β/Smad proteins （TGF-β/Smads）， confirming Sinisan's role in reversing the inflammation-to-cancer transformation. The current research status of Sinisan in precancerous lesions of the digestive system was thoroughly examined through the above three aspects， along with the identification of limitations and areas for improvement in current research. The aim is to provide a basis and support for future in-depth research on Sinisan， promote the development of new integrated treatment models combining TCM and Western medicine for precancerous lesions， and aid in the research and development of drugs related to precancerous lesions.

Objective:To analyze the effect of long noncoding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) on the radiosensitivity of cervical cancer cells and explore its regulatory role in the miR-455-3p/ nuclear factor-κB (NF-κB) signaling pathway.Methods:The expression levels of lncRNA SNHG16 and miR-455-3p in human normal cervical epithelial cells H8, human cervical cancer cells SiHa, and radioresistant cervical cancer cells SiHa-R were detected by real-time reverse transcription polymerase chain reaction. SiHa-R cells were transfected separately, and then given a single dose of 4 Gy X-ray irradiation and continued to be cultured for subsequent experiments. The cells in each group were named siRNA-NC, siRNA-SNHG16 (interfering lncRNA SNHG16), NC mimic, miR-455-3p mimic (overexpressing miR-455-3p), siRNA-SNHG16+inhibitor NC, and siRNA-SNHG16+miR-455-3p inhibitor groups, respectively. The survival fraction of SiHa-R cells was detected by clone formation assay. The apoptosis rate of SiHa-R cells was analyzed by flow cytometry. The expression levels of apoptotic proteins [cysteine-containing aspartate-specific protease (Caspase)-3, Caspase-9, Bax] and NF-κB signaling pathway related proteins [NF-κB p65, phosphorylated (p)-NF-κB p65, p-IκB (inhibitory protein of NF-κB)] were measured by Western blot. The targeting relationship between lncRNA SNHG16 and miR-455-3p was determined by dual luciferase reporter gene assay. Comparison among different groups was conducted by one-way ANOVA, and paired comparison was carried out by LSD t-test. Comparison between two groups was performed by t-test. Results:Compared with H8 cells, the expression levels of lncRNA SNHG16 were increased in SiHa and SiHa-R cells, and SiHa-R cells had a higher level than SiHa cells. The expression levels of miR-455-3p were decreased in SiHa and SiHa-R cells, and SiHa-R cells had a lower level than SiHa cells (all P<0.001). Compared with the siRNA-NC group, the survival fraction of SiHa-R cells in the siRNA-SNHG16 group was decreased, the radiosensitization ratio (SER) was 1.571 (>1), the apoptosis rate and levels of Caspase-3, Caspase-9, and Bax proteins were increased, while the levels of p-NF-κB p65 and p-IκB proteins were decreased (all P<0.001). lncRNA SNHG16 could target miR-455-3p. Compared with the NC mimic group, miR-455-3p level in the miR-455-3p mimic group was increased, cell survival fraction was decreased, the SER was 1.826 (>1), the apoptosis rate and the levels of Caspase-3, Caspase-9, Bax proteins were increased, and the levels of p-NF-κB p65 and p-IκB proteins were decreased (all P<0.001). Inhibition of miR-455-3p expression could weaken the effect of interfering with lncRNA SNHG16 expression on SiHa-R cell apoptosis, radiotherapy sensitivity, and NF-κB signaling pathway (all P<0.001). Conclusions:Interference with lncRNA SNHG16 expression could induce the apoptosis of cervical cancer cells and enhance their radiation sensitivity by regulating the miR-455-3p/NF-κB signaling pathway.

Objective The present study was designed to explore the inhibitory effects of the ADC drug Disitamab Vedotin(RC-48)on breast cancer cells with different HER-2 expression levels by utilizing a tumor organoid culture system.Methods Within the framework of the tumor organoid culture system,the breast cancer cell lines MCF-7(characterized by low HER-2 expression,Luminal A subtype)and BT-474(exhibiting high HER-2 expression,HER-2 positive subtype)were cultured independently and in various mixed ratios.The histological characteristics,as well as the expression levels and distribution of HER-2 in MCF-7 and BT-474 organoids,were analyzed via immunohistochemistry and immunofluorescence techniques.MCF-7 and BT-474 organoids were separately treated with Vedotin(RC-48),Disitamab,and Monomethyl auristatin E(MMAE).Additionally,a drug sensitivity test of Disitamab Vedotin(RC-48)was carried out on mixed MCF-7 and BT-474 cell ratios and on patient-derived breast cancer organoids,with the assessment conducted using the 3D-Glo method.Results In the tumor organoid culture system,immunohistochemistry and immunofluorescence analyses demonstrated that HER-2 was predominantly localized in the cell membrane.Specifically,BT-474 organoids exhibited robust HER-2 expression,while MCF-7 organoids displayed relatively low expression levels.When compared with MCF-7 organoids,RC48-ADC exerted a more pronounced inhibitory effect on BT-474 organoids,with IC50 values of 109.7 μg/mL and 2.792 μg/mL,respectively.The co-culture model further confirmed the bystander effect of RC-48,revealing that the ratio of HER-2-positive to HER-2-negative cells significantly influenced drug efficacy.Additionally,treatment with RC-48 led to a reduction in HER-2 expression in breast cancer organoids with diverse HER-2 expression levels.Conclusions The tumor organoid model can accurately mirror drug sensitivity and bystander effects.Within this model,RC-48 effectively inhibited HER-2 highly-expressing breast cancer cells,augmented the killing effect through the bystander mechanism,and downregulated HER-2 expression,thereby suggesting its potential for targeting HER2-associated breast cancer.

Breast cancer is a common clinical gy-necological tumor.According to the 2022 global cancer data statistics,breast cancer ranks second in terms of incidence among newly diagnosed cancer cases worldwide.Modern medicine often adopts surgical operation,chemotherapy,and other meth-ods,which have certain efficacy but also many problems such as high drug resistance rates and sig-nificant adverse reactions.Chinese patent medi-cines exhibit extensive anticancer effects.The study found that Shenyi Capsule,Pingxiao Capsule,and Zhenqi Fuzheng Granules were widely used in the treatment of breast cancer,exerting therapeu-tic effects on breast cancer by inhibiting cell prolif-eration,invasion,and metastasis,suppressing an-giogenesis,reversing cellular drug resistance,and inhibiting precancerous lesions.Meanwhile,the oral administration of Chinese patent medicines in combination with other traditional Chinese medi-cine(TCM)compounds,TCM decoctions,or mod-ern medical treatments can improve patients' quali-ty of life and reduce adverse reactions.Currently,there are numerous studies on the treatment of breast cancer with Chinese patent medicines,but a systematic summary is lacking.Therefore,this study conducted a systematic review of the mecha-nisms of action and clinical applications of Chinese patent medicines as adjuvant therapy for breast cancer,aiming to provide guidance for clinical medi-cation.

Triple-negative breast cancer (TNBC) represents an aggressive breast cancer subtype with poor prognosis and limited targeted treatment options. This investigation examined the anti-cancer potential of Caerulomycin A (Cae A), a natural compound derived from marine actinomycetes, against TNBC. Cae A demonstrated selective inhibition of viability and proliferation in TNBC cell lines, including 4T1, MDA-MB-231, and MDA-MB-468, through apoptosis induction. Mechanistic analyses revealed that the compound induced sustained endoplasmic reticulum (ER) stress and subsequent upregulation of C/EBP homologous protein (CHOP) expression, resulting in mitochondrial damage-mediated apoptosis. Inhibition of ER stress or CHOP expression knockdown reversed mitochondrial damage and apoptosis, highlighting the essential role of ER stress and CHOP in Cae A's anti-tumor mechanism. Both oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) decreased in TNBC cells following Cae A treatment, indicating reduced mitochondrial respiratory and glycolytic capacities. This diminished energy metabolism potentially triggers ER stress and subsequent apoptosis. Furthermore, Cae A exhibited significant anti-tumor effects in the 4T1 tumor model in vivo without apparent toxicity. The compound also effectively inhibited human TNBC organoid growth. These results indicate that Cae A may serve as a potential therapeutic agent for TNBC, with its efficacy likely mediated through the disruption of glucose metabolism and the induction of ER stress-associated apoptosis.
Humans ; Endoplasmic Reticulum Stress/drug effects* ; Triple Negative Breast Neoplasms/genetics* ; Apoptosis/drug effects* ; Cell Line, Tumor ; Female ; Animals ; Glucose/metabolism* ; Mice ; Cell Proliferation/drug effects* ; Transcription Factor CHOP/genetics* ; Antineoplastic Agents/pharmacology* ; Mitochondria/metabolism* ; Mice, Inbred BALB C

Objective: To evaluate the efficacy and safety of the single-use hemoperfusion device (UA230) in treating refractory gout (RG) via plasma perfusion. Methods: Thirty-four RG patients aged 18-65 years were recruited and randomly divided into a control group (febuxostat therapy, n=17) and an experimental group (plasma perfusion combined with febuxostat therapy, n=17). Differences in serum uric acid (SUA) levels and urate-lowering rates between the two groups were analyzed using t-tests. Between-group differences in incidence of adverse reactions were analyzed using chi-square tests. Results: At 7 and 14 days post-treatment, SUA levels in the experimental group were significantly lower than those in the control group, with a higher urate-lowering rate (all P<0.05). However, no statistically significant differences in SUA levels or urate-lowering rate were observed at 28 days post-treatment (all P>0.05). The incidence of adverse reactions showed no significant difference between the two groups (χ =0.15, P>0.05). Conclusion: The single-use hemoperfusion device (UA230), combined with plasma perfusion technology, is a safe and effective treatment for RG. It may serve as a novel therapeutic approach for RG patients in clinical practice.