Progress in the study of antibody-drug conjugates for the treatment of cervical cancer.

Cervical cancer is the second most prevalent malignancy affecting women's health globally, and the number of morbidity and mortality from cervical cancer continues to rise worldwide. The 5-year survival rate of patients with recurrent or metastatic cervical cancer is significantly reduced, and existing treatment modalities have low efficacy and high adverse effects, so there is a strong need for new, effective, and well-tolerated therapies. Antibody-drug conjugates (ADCs) are a new targeted therapeutic modality that can efficiently kill tumor cells. This review aims to summarize the composition, research, and development history and mechanism of action of ADCs, to review the research progress of ADCs in the treatment of cervical cancer, and to summarize and prospect the application of ADCs.

The Role of CXCL11 and its Receptors in Cancer: Prospective but Challenging Clinical Targets.

Chemokine ligand 11 is a member of the CXC chemokine family and exerts its biological function mainly through binding to CXCR3 and CXCR7. The CXCL11 gene is ubiquitously overexpressed in various human malignant tumors; however, its specific mechanisms vary among different cancer types. Recent studies have found that CXCL11 is involved in the activation of multiple oncogenic signaling pathways and is closely related to tumorigenesis, progression, chemotherapy tolerance, immunotherapy efficacy, and poor prognosis. Depending on the specific expression of its receptor subtype, CXCL11 also has a complex 2-fold role in tumours; therefore, directly targeting the structure-function of CXCL11 and its receptors may be a challenging task. In this review, we summarize the biological functions of CXCL11 and its receptors and their roles in various types of malignant tumors and point out the directions for clinical applications.

CXCL11 is found in many types of cancer and affects how cancer cells grow and respond to treatments. This paper delves into the intricate dance between CXCL11 and its receptors in various types of cancer. Like a versatile actor playing different roles on stage, CXCL11 can either promote or hinder cancer growth depending on its interaction with specific receptors. Understanding how CXCL11 works could help develop new treatments for cancer, but it's a complex challenge because CXCL11 can have different effects depending on the type of cancer and which receptors it binds to.

Expression and correlation of COX-2 and NUCB1 in colorectal adenocarcinoma.

Objective: To investigate the expression and correlation of COX-2 and NUCB1 in colorectal adenocarcinoma and adjacent tissues. Methods: The expression of COX-2 and NUCB1 and their effects on prognosis were predicted using bioinformatics. Immunohistochemistry was used to identify the expression of two molecules in 56 cases of colorectal adenocarcinoma and the surrounding tissues. The expression of two molecules and their association with clinicopathological variables were examined using the chi-square test. The association between COX-2 and NUCB1 was investigated using the Spearman correlation test. Results: The STRING database revealed that COX-2 and NUCB1 were strongly linked. According to the UALCAN and HPA database, COX-2 was upregulated while NUCB1 was downregulated in colorectal adenocarcinoma, both at the protein and gene levels. The OS times for COX-2 and NUCB1 high expression, however, exhibited the same patterns. The rate of positive COX-2 immunohistochemical staining in cancer tissues was 69.64% (39/56), which was significantly higher than the rate in healthy tissues 28.57% (16/56). NUCB1 was expressed positively in cancer tissues at a rate of 64.29% (36/56) compared to just 19.64% (11/56) in neighboring tissues. The positive expression levels of COX-2 and NUCB1 were both closely related to clinical stage, differentiation degree, and lymphatic metastases (P < 0.05). In colorectal cancer, COX-2 and NUCB1 expression were significantly correlated (rs = 0.6312, P < 0.001). Conclusion: Both COX-2 and NUCB1 are overexpressed and significantly associated in colorectal adenocarcinoma.

HMGA2 promotes nasopharyngeal carcinoma progression and is associated with tumor resistance and poor prognosis.

Nasopharyngeal carcinoma (NPC), as one of the most prevalent malignancies in the head and neck region, still lacks a complete understanding of its pathogenesis. Presently, radiotherapy, concurrent chemoradiotherapy, and targeted therapy stand as the primary modalities for treating NPC. With advancements in medicine, the cure rates for nasopharyngeal carcinoma have been steadily increasing. Nevertheless, recurrence and metastasis persist as the primary reasons for treatment failure. Consequently, a profound exploration of the molecular mechanisms underlying the occurrence and progression of nasopharyngeal carcinoma, along with the exploration of corresponding therapeutic approaches, becomes particularly imperative in the quest for comprehensive solutions to combat this disease. High mobility group AT-hook 2 (HMGA2) is a pivotal protein capable of altering chromatin structure, regulating gene expression, and influencing transcriptional activity. In the realm of cancer research, HMGA2 exhibits widespread dysregulation, playing a crucial role in nearly all malignant tumors. It is implicated in various tumorigenic processes, including cell cycle regulation, cell proliferation, epithelial-mesenchymal transition, angiogenesis, tumor invasion, metastasis, and drug resistance. Additionally, HMGA2 serves as a molecular marker and an independent prognostic factor in certain malignancies. Recent studies have increasingly unveiled the critical role of HMGA2 in nasopharyngeal carcinoma (NPC), particularly in promoting malignant progression, correlating with tumor resistance, and serving as an independent adverse prognostic factor. This review focuses on elucidating the oncogenic role of HMGA2 in NPC, suggesting its potential association with chemotherapy resistance in NPC, and proposing its candidacy as an independent factor in nasopharyngeal carcinoma prognosis assessment.

Lactate: The Mediator of Metabolism and Immunosuppression.

The Warburg effect, one of the hallmarks of tumors, produces large amounts of lactate and generates an acidic tumor microenvironment via using glucose for glycolysis. As a metabolite, lactate not only serves as a substrate to provide energy for supporting cell growth and development but also acts as an important signal molecule to affect the biochemical functions of intracellular proteins and regulate the biological functions of different kinds of cells. Notably, histone lysine lactylation (Kla) is identified as a novel post-modification and carcinogenic signal, which provides the promising and potential therapeutic targets for tumors. Therefore, the metabolism and functional mechanism of lactate are becoming one of the hot fields in tumor research. Here, we review the production of lactate and its regulation on immunosuppressive cells, as well as the important role of Kla in hepatocellular carcinoma. Lactate and Kla supplement the knowledge gap in oncology and pave the way for exploring the mechanism of oncogenesis and therapeutic targets. Research is still needed in this field.

Design and Implementation of Chinese Common Braille Translation System Integrating Braille Word Segmentation and Concatenation Rules.

An important sign of the accessibility of Braille information is the realization of the mutual translation between Chinese and the Braille. Due to the irregularity and uncertainty of the Prevailing Mandarin Braille, coupled with the lack of a large-scale Braille corpus, the quality of Chinese-Braille translation seems to be poor. In July 2018, the National Language Commission released the "Chinese Common Braille Scheme" and advocated replacing the "Prevailing Mandarin Braille." Aimed at improving translation accuracy, this research, which is based on the self-built Chinese Common Braille corpus and combined with the HanLP (Han Language Processing) dictionary and the Chinese-Braille word corpus (a Braille word segmentation and concatenation dictionary for generating a unigram language model), uses the n-gram language model to design and implement a Chinese-Braille intertranslation system that integrates Chinese and Braille Word Segmentation and Concatenation Rules. More importantly, this research proposes an experimental plan for improving the Braille Word Segmentation and Concatenation Rules using a Chinese-Braille word corpus. Experiments show that in the field of educational literature, the accuracy rate of translation from Chinese to Chinese Common Braille has reached 95.01%, and the accuracy of Chinese Common Braille to Chinese translation has reached 90.15%.

ATF1/miR-214-5p/ITGA7 axis promotes osteoclastogenesis to alter OVX-induced bone absorption.

BACKGROUND: The dynamic balance of osteoblast and osteoclast is critical for bone homeostasis and overactive osteoclastic function may lead to osteoporosis. Activating transcription factor 1 (ATF1) is involved in osteoclastogenesis. However, the detailed mechanisms remain to be explored. METHODS: RAW264.7 cells were used and induced toward osteoclast by RANKL administration. We performed flow cytometry, CCK-8 assay and tartrate-resistant acid phosphatase (TRAP) staining to examine cell apoptosis, proliferation and differentiation of RAW264.7 cells, respectively. Mice were subjected to ovariectomy to induce osteoporosis. Micro CT, HE staining and TRAP staining were performed to evaluate bone loss in the OVX mouse model. Bioinformatics methods, luciferase assays and Chromatin Immunoprecipitation (ChIP) were used to predict and validate the interaction among ATF1, miR-214-5p, and ITGA7. RESULTS: ATF1 and miR-214-5p were up-regulated while ITGA7 was inhibited in RANKL-induced osteoclasts. MiR-214-5p was transcriptionally activated by ATF1. ATF1 knockdown suppressed osteoclast formation by miR-214-5p inhibition. ITGA7 was the direct target of miR-214-5p. Knockdown of miR-214-5p abolished osteoclastogenesis, which was reversed by ITGA7 knockdown. In OVX model, miR-214-5p knockdown suppressed osteoclast differentiation and prevented bone loss. CONCLUSION: ATF1/miR-214-5p/ITGA7 axis regulated osteoclast formation both in vivo and in vitro, thereby affecting OVX-induced bone resorption in mice. Knockdown of ATF1 might be a promising strategy to manage osteoporosis.

Identification of ferroptosis-related genes as potential biomarkers of tongue squamous cell carcinoma using an integrated bioinformatics approach.

Tongue squamous cell carcinoma (TSCC) is one of the deadliest cancers of the head and neck, but the role of the ferroptosis pathway in its development is still unknown. In this study we explored the pathogenetic mechanisms associated with ferroptosis in TSCC. We identified differentially expressed genes (DEGs) of TSCC patients and used gene ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) to annotate, visualize, and integrate these DEGs. Receiver operating characteristic curve (ROC) analysis was performed, and the STRING database was used to construct a protein-protein interaction network to evaluate the predictive value of ferroptosis-related DEGs. A total of 219 DEGs were identified and GO, KEGG, and GSEA showed that extracellular matrix (ECM)-receptor interaction and interleukin (IL)-17 signaling pathways were substantially upregulated in TSCC. Univariate Cox analysis revealed that high expression of CA9, TNFAIP3, and NRAS were predictive of a worse outcome. We then constructed a prognostic model that predicted survival in the validation cohort at 1 year and 32 months. Finally, 60 cases of tongue carcinoma and normal tissues were collected, and immunohistochemistry was used to detect the expression of CA9. We found that CA9 was strongly expressed in tongue carcinoma tissues and absent in adjacent tissues. Overall, we found that ferroptosis-related genes may affect TSCC prognosis through the ECM-receptor interaction and IL-17 signaling pathways. Additionally, immunohistochemistry confirmed that CA9 was highly expressed in tongue carcinoma tissues, and a model based on ferroptosis-related genes showed a good ability to predict overall survival in TSCC.

Evaluation of GeneXpert vanA/vanB in the early diagnosis of vancomycin-resistant enterococci infection.

PURPOSE: Vancomycin-resistant enterococci infection is a worrying worldwide clinical problem. To evaluate the accuracy of GeneXpert vanA/vanB in the diagnosis of VRE, we conducted a systematic review in the study. METHODS: Experimental data were extracted from publications until May 03 2021 related to the diagnostic accuracy of GeneXpert vanA/vanB for VRE in PubMed, Embase, Web of Science and the Cochrane Library. The accuracy of GeneXpert vanA/vanB for VRE was evaluated using summary receiver to operate characteristic curve, pooled sensitivity, pooled specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio. RESULTS: 8 publications were divided into 3 groups according to two golden standard references, vanA and vanB group, vanA group, vanB group, including 6 researches, 5 researches and 5 researches, respectively. The pooled sensitivity and specificity of group vanA and vanB were 0.96 (95% CI, 0.93-0.98) and 0.90 (95% CI, 0.88-0.91) respectively. The DOR was 440.77 (95% CI, 37.92-5123.55). The pooled sensitivity and specificity of group vanA were 0.86 (95% CI, 0.81-0.90) and 0.99 (95% CI, 0.99-0.99) respectively, and those of group vanB were 0.85 (95% CI, 0.63-0.97) and 0.82 (95% CI, 0.80-0.83) respectively. CONCLUSION: GeneXpert vanA/vanB can diagnose VRE with high-accuracy and shows greater accuracy in diagnosing vanA.

Evaluation of Xpert GBS assay and Xpert GBS LB assay for detection of Streptococcus agalactiae.

BACKGROUND: Group B Streptococcal (GBS) infection is the primary agent of neonatal morbidity and mortality. Rapid and simple methods to detect GBS are Xpert GBS and GBS LB assays based on real-time polymerase chain reaction (PCR). However, since the diagnostic accuracy of the two techniques in diagnosing GBS remains unclear, we designed this study to appraise the diagnostic accuracy of the aforementioned. METHODS: A systematic search of all literature published before July 16, 2020 was conducted using Embase, PubMed, Web of Science, and Cochrane Library. The study quality was evaluated through Review Manager 5.3. Accordingly, data extracted in the included studies were analyzed using Meta-DiSc 1.4 and Stata 12.0 software. The diagnosis odds ratio (DOR) and bivariate boxplot were utilized to evaluate the heterogeneity. Publication bias was appraised by using Deeks' funnel plot. RESULTS: A total of 13 studies were adopted and only 19 sets of data met the criteria. The sensitivity and specificity of Xpert GBS were 0.91 (95% CI 0.89-0.92) and 0.93 (95% CI 0.92-0.94). The area under the curve (AUC) was 0.9806. The sensitivity and specificity results of Xpert GBS LB were 0.96 (95% CI 0.95-0.98) and 0.94 (95% CI 0.92-0.95), respectively. The AUC was 0.9950. No publication bias was found. CONCLUSIONS: The Xpert GBS and GBS LB assays are valuable alternative methods with high sensitivity and specificity. However, determining whether they can be used as clinical diagnostic standards for GBS is essential for the future.

LncRNA SNHG15 modulates gastric cancer tumorigenesis by impairing miR-506-5p expression.

The gastric cancer (GC) patients commonly have a poor prognosis due to its invasiveness and distant metastasis. Growing evidence proved that aberrant long non-coding RNAs (lncRNAs) expression contributes to tumor development and progression. LncRNA SNHG15 has been reported to be involved in many different kinds of cancer, while its role in GC remains unclear. In the present study, we found that SNHG15 was up-regulated in GC tissues and cell lines. Silencing SNHG15 suppressed proliferation migration, invasion and promoted apoptosis of AGS cells. More importantly, microRNA-506-5p (miR-506-5p) was predicted as a direct target of SNHG15 by binding its 3'-UTR and further verified using luciferase reporter assay. Meanwhile, the results of rescue experiments revealed that knockdown of miR-506-5p expression reversed the functional effects of SNHG15 silenced cell proliferation, migration, invasion and apoptosis. In conclusion, our findings revealed that SNHG15 executed oncogenic properties in GC progression through targeting miR-506-5p, which might provide a novel target for the GC treatment.

MicroRNA­129 inhibits colorectal cancer cell proliferation, invasion and epithelial­to­mesenchymal transition by targeting SOX4.

Colorectal cancer (CRC) is one of the most common digestive tract cancers and ~90% of CRC­related deaths are caused by metastasis. MicroRNA (miR)­129 has been reported to be involved in the metastasis of various malignant tumors. However, the role of miR­129 in CRC metastasis remains unclear. The purpose of the present study was to identify the potential functions and mechanisms of action of miR­129 in CRC progression. The expression of miR­129 and sex­determining region Y­related high­mobility group­box 4 (SOX4) was determined in CRC tissues or cell lines by reverse transcription­quantitative PCR, western blot or immunofluorescence assays. The mechanism underlying the role of miR­129 in CRC progression was assessed by MTT, wound healing, Transwell, western blot and dual­luciferase report assays. The results revealed that miR­129 was significantly decreased, whereas SOX4 was increased, in CRC tissues and cell lines. SW620 and SW480 cells exhibited a higher proliferation, migration and invasion capacity compared with NCM460 cells. miR­129 overexpression significantly inhibited cell proliferation, migration, invasion and epithelial­to­mesenchymal transition (EMT), and it activated the nuclear factor (NF)­κB signaling pathway in CRC cells, while the inhibition of miR­129 exerted opposite effects. Additionally, SOX4 was identified as a direct target gene of miR­129. Taken together, the findings of the present study suggested that miR­129 may act as a tumor suppressor in CRC by inhibiting CRC cell proliferation, migration, invasion and EMT, in part through targeting the 3'­untranslated region of SOX4 mRNA, and the mechanism may involve activation of the NF­κB signaling pathway.

TELO2 induced progression of colorectal cancer by binding with RICTOR through mTORC2.

Colorectal cancer (CRC) is a common cancer worldwide, and its treatment strategies are limited. The underlying mechanism of CRC progression remains to be determined. Telomere maintenance 2 (TELO2) is a mTOR­interacting protein. Both the role and molecular mechanism of TELO2 in cancer progression remain unknown. In this study, the gene expression database of normal and tumor tissue, in addition to western blot analysis, and immunohistochemistry (IHC) were used to determine the expression and location of TELO2 in CRC and normal tissues. Clinical features of a tissue array were collected and analyzed. WST­1, soft agar, flow cytometry, wound healing, and invasion assays were employed to verify the role of TELO2 in the growth, cell cycle, migration, and invasion of CRC cells. The correlation between TELO2 and RICTOR (rapamycin­insensitive companion of mTOR) was analyzed by bioinformatics, IHC, and immunoprecipitation. Normal and serum­deprived cells were collected to detect the protein level of TELO2 and its downstream effectors. The results revealed that TELO2 was significantly upregulated in CRC, and TELO2 inhibition significantly restrained the growth, cell cycle, and metastasis of CRC cells. TELO2 overexpression correlated with age, lymph node metastasis, and TNM stage of CRC patients. In addition, TELO2 was positively correlated with RICTOR in CRC and induced tumor progression mainly via RICTOR with serum in culture. RICTOR induced the degradation of TELO2 upon serum deprivation in an mTOR­independent manner. These findings indicate that TELO2 promotes tumor progression via RICTOR in a serum­dependent manner, which may be a potential therapeutic target for CRC.

Lupeol inhibits osteosarcoma progression by up-regulation of HMGA2 via regulating miR-212-3p.

BACKGROUND: Osteosarcoma (OS) is a common severe illness globally. Lupeol has been reported to participate in the pathophysiologic properties of various cancers, including OS. This study aimed to explore the effects of lupeol on proliferation, invasion, and apoptosis on OS cells and the underlying mechanism. METHODS: The cell viability of OS cells was determined by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The expression levels of miR-212-3p and high-mobility group AT-hook 2 (HMGA2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in OS cells. The cell apoptosis and invasion were detected by flow cytometry and transwell invasion assays, respectively. The functional target of miR-212-3p was predicted by online software and confirmed by luciferase reporter assay. The protein level of HMGA2 was measured by western blot analysis. RESULTS: Lupeol suppressed cell viability and invasion, and promoted apoptosis by upregulating the expression of miR-212-3p in OS cells. Knockdown of miR-212-3p restored the anti-tumor effect of lupeol. Interestingly, miR-212-3p directly targeted HMGA2 and suppressed its expression. Moreover, HMGA2 reversed the inhibited impact on viability and invasion, and the promoted effect on apoptosis induced by upregulation of miR-212-3p. Also, lupeol administration exerts its anti-tumor effect by overexpression of miR-212-3p to suppress the expression of HMGA2 in OS cells. CONCLUSION: Lupeol inhibited OS progression by modulating the miR-212-3p/HMGA2 axis in vitro.

Risk Factors for Cancer-specific Mortality and Cardiovascular Mortality in Patients With Diffuse Large B-cell Lymphoma.

BACKGROUND: The purpose of this study was to assess the risk factors for cancer-specific mortality and cardiovascular mortality in patients with diffuse large B-cell lymphoma (DLBCL). PATIENTS AND METHODS: A retrospective cohort study involving patients with DLBCL who were registered in the Surveillance, Epidemiology, and End Results (SEER) database was performed. The risk factors for cancer-specific mortality and cardiovascular mortality were analyzed using the competing risk regression model. RESULTS: A total of 62,950 patients with DLBCL were enrolled, of which 23,302 (37.50%) died of cancer and 2940 (4.70%) died of cardiovascular disease. The competing risk multivariate analysis displayed that age at diagnosis (hazard ratio [HR], 1.033; 95% confidence interval [CI], 1.032-1.034), marriedstatus (HR, 1.293; 95% CI, 1.241-1.347), black race (HR, 1.079; 95% CI, 1.021-1.139), and tumor stage (II: HR, 1.143; 95%CI, 1.095-1.192; III: HR, 1.459; 95% CI, 1.395-1.526; IV: HR, 1.961; 95% CI. 1.889-2.035) were the risk factors for cancer-specific mortality, but not female gender (HR, 0.938; 95% CI, 0.913,0.965) or treatment modalities (chemotherapy: HR, 0.522; 95% CI, 0.505-0.540; radiotherapy: HR, 0.782; 95% CI, 0.728-0.839; chemotherapy + radiotherapy: HR, 0.422; 95% CI, 0.403-0.441). Age at diagnosis (HR, 1.059; 95% CI, 1.055-1.062) and black race (HR, 1.246; 95% CI, 1.067-1.456) were the risk factors for cardiovascular mortality rather than female gender (HR, 0.803; 95% CI, 0.743-0.867) and married status (HR, 0.841; 95% CI, 0.745-0.950). CONCLUSIONS: Age at diagnosis, married status, black race, and higher tumor stage are associated with an increased risk of cancer-specific mortality in patients with DLBCL, whereas age at diagnosis and black race are associated with a higher risk of cardiovascular mortality.

Combining pretreatment plasma Epstein-Barr virus DNA level and cervical node necrosis improves prognostic stratification in patients with nasopharyngeal carcinoma: A cohort study.

This study aimed to evaluate the prognostic value of combining pretreatment Epstein-Barr virus (EBV) DNA level and cervical node necrosis (CNN) for patients with nasopharyngeal carcinoma (NPC) receiving intensity-modulated radiotherapy (IMRT). A total of 607 incident nonmetastatic NPC patients treated with IMRT ± chemotherapy were reviewed. Patients were divided into four groups based on EBV DNA level and CNN status. The primary endpoint was progression-free survival (PFS). Kaplan-Meier curves with log-rank test were applied to compare survival outcomes and the Cox proportional model was used to identify independent prognostic factors. Pretreatment EBV DNA level and CNN status were independent prognostic factors. Patients in the low-level EBV DNA group or non-CNN group had significantly better 5-year PFS. Multivariate analyses demonstrated that CNN was an independent prognostic factor for overall survival (OS) (HR = 1.927, 95% CI: 1.129-3.290, P = .016), PFS (HR = 1.492, 95% CI: 1.005-2.214, P = .047), distant metastasis-free survival (DMFS) (HR = 1.661, 95% CI: 1.044-2.644, P = .032), but not locoregional relapse-free survival. EBV DNA levels correlated significantly with CNN with a correlation coefficient of .324 (P < .001). Compared with low-level EBV DNA and non-CNN grouping, high-level EBV DNA and CNN grouping had poor PFS. The combined classification was an independent prognostic factor for OS (P < .001), PFS (P = .001), and DMFS (P = .018). Pretreatment plasma EBV DNA level and CNN status both closely correlated with prognosis of NPC patients in the IMRT era. Combined EBV DNA level and CNN status improves risk stratification and prognostic value.

KAI1 overexpression promotes apoptosis and inhibits proliferation, cell cycle, migration, and invasion in nasopharyngeal carcinoma cells.

OBJECTIVES: The purpose of this study is to characterize the effect of KAI1 overexpression on the biological behavior of nasopharyngeal carcinoma (NPC) cells. BACKGROUND: Nasopharyngeal carcinoma is a highly malignant tumor with a high rate of incidence in China. Currently, there are no ideal therapeutic options for patients with NPC, but a targeted therapy would have great potential for treating it. Therefore, there is an urgent need for novel therapeutic targets to provide new options for treating NPC. The KAI1 gene was originally identified as a metastasis suppressor gene for advanced human cancer. In NPC cell lines and tissues, the expression of KAI1 decreased as the metastatic potential of cells increased, but its potential as a therapeutic target has not been elucidated. METHODS: Non-transformed nasopharyngeal epithelium cell NP69 and NPC cell line C666-1 were cultured and KAI1 expression in these cells was detected by qRT-PCR and Western blot. After the transfection of KAI1-pCDNA3.1 to NP69 and C666-1, the KAI1 expression in these cells was detected by qRT-PCR and Western blot, the proliferation was performed by MTS, the cell cycle and apoptosis were performed by flow cytometry, the migration and invasion were examined by transwell. RESULTS: Our results showed that KAI1 was significantly upregulated in C666-1 cells compared to that in NP69 cells. In addition, KAI1 overexpression significantly inhibited the proliferation, cell cycle, migration, and invasion, and promoted apoptosis of C666-1 cells, but had no significant effect on NP69 cells. CONCLUSION: Our findings suggest that KAI1 overexpression promotes apoptosis and inhibits proliferation, cell cycle, migration, and invasion in NPC cells. We hypothesize that KAI1 overexpression could be a potential therapeutic target for NPC.

[Identification of major components of traditional Chinese medicine Naodesheng tablet by HPLC-DAD-MS(n)].

OBJECTIVE: To identify the major components of traditional Chinese medicine Naodesheng tablet. METHODS: A HPLC-DAD-MS(n) based method was developed to analyze and identify the major components of Naodesheng tablet. Separation was performed on an Agilent Zorbax SB-C(18) column (4.6 mm X 250 mm, i.d, 5 µm) with mobile phase consisting of water with 0.05 % formic acid and acetonitrile as gradient eluent at the flow rate of 0.5 ml.min(-1). RESULTS: A total of 43 components were detected, among which 22 were identified by comparing their UV absorption profiles, the information of molecular Glucosyl puerarin weights, and structures provided by ESI-MS(n) with those of available standards and reference data, such as Safflor yellow A, 4'-O-Glucosyl puerarin, 3'-hydroxypuerarin, Genistein-8-C-apiosyl (1-6) glucoside, Puerarin, 6"-O-xylosyl puerarin, 6"-O-apiosyl puerarin, 3'-methoxy puerarin, 3'-methoxy-6"-o-xylosyl puerarin, Daidzin, Genistin, Pueroside A, Notoginsenoside R(1), Ginsenoside Re, Ginsenoside Rg1,Daidzein,Biochanin A,Ginsenoside Rb(1), Ginsenoside Rc, Ginsenoside Rb(2), Ginsenoside Rb(3), Ginsenoside Rd. CONCLUSION: The proposed method can identify the main components of Naodesheng tablet and provide information for the quality control of this medicine.

Virtual separation of phytochemical constituents by their adduct-ion patterns in full mass spectra.

In the present study, a tool called classifier for traditional Chinese medicine (CTCM) was developed to facilitate the discrimination of phytochemical constituents in two-dimensional datasets of liquid chromatography/mass spectrometry (LC/MS). Based on the full mass spectral characteristics of components in a mixture, particularly their adduct-ion patterns, an entire LC/MS dataset can be separated into several sub-datasets, each corresponding to one or several types of natural products. CTCM has been verified using 24 standard compounds and successfully applied in two previously reported LC/MS datasets, which confirmed the capability of proposed tool to extract adduct-ion patterns from LC/MS datasets. Moreover, the LC/MS dataset of a Wei-Fu-Chun (WFC) tablet, a prescription drug consisting of three crude herbs used for the treatment of enteric diseases, was analyzed using CTCM. The analysis indicated that the compounds in WFC could be split into three groups, with the main constituents including saponins from Radix Ginseng Rubra, flavonoids from Fructus aurantii, and phenolic compounds from Isodon amethystoides. The major compounds in the three groups were either positively identified or tentatively characterized by multi-stage and high resolution MS. The proposed tool provides a novel approach for processing the LC/MS datasets of complex samples, such as traditional Chinese medicine and botanical drugs.