The risk of breast cancer and gynecologic malignancies after ovarian stimulation: Meta-analysis of cohort study.

The effects of ovarian stimulation on breast and gynecological tumor incidence remain controversial. Therefore, the aim of this meta-analysis was to study the risk of cancer in ovarian stimulation. Of the 22713 studies initially identified, 28 were eligible for inclusion. The results revealed that the impact of ovarian cancer (RR = 1.33, [1.05; 1.69]) and cervical cancer (RR = 0.67, [0.46; 0.97]) is significant among the overall effects. In subgroup analysis, in the nulliparous population (RR = 0.81 [0.68; 0.96]) was the protective factor for the breast cancer. In the Caucasians subgroup (RR = 1.45, [1.12; 1.88]), the ovarian cancer incidence was statistically significant. In the Asian subgroup (RR = 1.51, [1.00; 2.28]), the endometrial cancer incidence was statistically significant. In the subgroup of Asians (RR = 0.55 [0.44; 0.68]) and the multiparous population (RR = 0.31, [0.21; 0.46]), them can be the statistically protective factor for the cervical cancer.

Efficacy and safety of traditional Chinese medicine for cancer-related fatigue: a systematic literature review of randomized controlled trials.

BACKGROUND: Cancer-related fatigue (CRF) is an extremely common and long-term condition that affects the physical and mental health of oncology patients. While the treatment for CRF with western medicine and non-pharmacological therapy remains uncertain and challenging, traditional Chinese medicine (TCM) has become a trending option for the patients. Based on the findings from randomized controlled trials (RCTs), this study aims to identify and evaluate the evidence about the efficacy and safety of TCM for CRF. METHODS: A systematic literature search was conducted according to the PRISMA literature research guidelines. Seven electronic databases including PubMed, the Cochrane Library, Embase, Web of Science, Scopus, China National Knowledge Infrastructure (CNKI) and Wanfang database were searched to identify RCTs which investigated TCM in the treatment of CRF published since inception to December 2022. RCTs comparing TCM with no treatment, placebo, or pharmacological interventions were considered eligible for this review. The Consolidated Standards of Reporting Trials Statement extensions for Chinese herbal medicine Formulas (CONSORT-CHM) and the Cochrane Collaboration's Risk of Bias tool were used in this review to evaluate the quality and the risk of bias of all included trials. RESULTS: A total of 82 RCTs were included in this review, regardless of whether they were published in English or Chinese. After data extraction and results evaluation, 78 trials demonstrated overall efficacy in using TCM for CRF patients compared with the control group, in which 33 trials showed that the efficacy rate was statistically significant (p < 0.05 or p < 0.01). TCM was also shown to be beneficial in improving the scores of relevant scales (e.g., PFS, QoL, TCM syndrome score, other fatigue scales etc.) or physical tests indicators (e.g., cytokines, blood test etc.). The most common herbs found in Chinese medicine were Astragali Radix, Ginseng Radix and Codonopsis Radix. Some TCM products, such as Kangai Injection, Buzhong Yiqi Decoction and Shenqi Fuzheng Injection could provide a reference for medication in this review. A range of non-serious, reversible adverse effects associated with the use of TCM was also reported. However, the result of evaluation showed that none of the trials fully met all the CONSORT-CHM criteria, the quality of included trials was generally poor and the risk of bias was mostly uncertain. CONCLUSION: There is some evidence supporting the efficacy and safety of TCM in managing CRF in this systematic review. However, no clear conclusion can be made due to the inadequate reporting of efficacy and adverse reactions. In view of some concerns about the existing evidence after the evaluation, it is essential to standardize the comprehensive identification and efficacy measurement standards, improve the quality of RCTs and conduct more multicomponent therapies to provide an updated reference for CRF patients medication in the future. The protocol of this systematic review has been registered on PROSPERO (CRD42023413625). [ https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023413625 ].

The preimplantation genetic testing for monogenic disorders strategy for blocking the transmission of hereditary cancers through haplotype linkage analysis by karyomapping.

PURPOSE: Providing feasible preimplantation genetic testing strategies for monogenic disorders (PGT-M) for prevention and control of genetic cancers. METHODS: Inclusion of families with a specific pathogenic mutation or a clear family history of genetic cancers. Identification of the distribution of hereditary cancer-related mutations in families through genetic testing. After a series of assisted reproductive measures such as down-regulation, stimulation, egg retrieval, and in vitro fertilization, a biopsy of trophectoderm cells from a blastocyst was performed for single-cell level whole-genome amplification (WGA). Then, the detection of chromosomal aneuploidies was performed by karyomapping. Construction of a haplotype-based linkage analysis to determine whether the embryo carries the mutation. Meanwhile, we performed CNV testing. Finally, embryos can be selected for transfer, and the results will be verified in 18-22 weeks after pregnancy. RESULTS: Six couples with a total of 7 cycles were included in our study. Except for cycle 1 of case 5 which did not result in a transferable embryo, the remaining 6 cycles produced transferable embryos and had a successful pregnancy. Four couples have had amniotic fluid tests to confirm that the fetus does not carry the mutation, while 1 couple was not tested due to insufficient pregnancy weeks. And the remaining couples had to induce labor due to fetal megacystis during pregnancy. CONCLUSION: Our strategy has been proven to be feasible. It can effectively prevent transmission of hereditary cancer-related mutations to offspring during the prenatal stage.

Ultrasound Image Classification of Thyroid Nodules Based on Deep Learning.

A thyroid nodule, which is defined as abnormal growth of thyroid cells, indicates excessive iodine intake, thyroid degeneration, inflammation, and other diseases. Although thyroid nodules are always non-malignant, the malignancy likelihood of a thyroid nodule grows steadily every year. In order to reduce the burden on doctors and avoid unnecessary fine needle aspiration (FNA) and surgical resection, various studies have been done to diagnose thyroid nodules through deep-learning-based image recognition analysis. In this study, to predict the benign and malignant thyroid nodules accurately, a novel deep learning framework is proposed. Five hundred eight ultrasound images were collected from the Third Hospital of Hebei Medical University in China for model training and validation. First, a ResNet18 model, pretrained on ImageNet, was trained by an ultrasound image dataset, and a random sampling of training dataset was applied 10 times to avoid accidental errors. The results show that our model has a good performance, the average area under curve (AUC) of 10 times is 0.997, the average accuracy is 0.984, the average recall is 0.978, the average precision is 0.939, and the average F1 score is 0.957. Second, Gradient-weighted Class Activation Mapping (Grad-CAM) was proposed to highlight sensitive regions in an ultrasound image during the learning process. Grad-CAM is able to extract the sensitive regions and analyze their shape features. Based on the results, there are obvious differences between benign and malignant thyroid nodules; therefore, shape features of the sensitive regions are helpful in diagnosis to a great extent. Overall, the proposed model demonstrated the feasibility of employing deep learning and ultrasound images to estimate benign and malignant thyroid nodules.

MAIT cells and their implication in human oral diseases.

OBJECTIVE: Mucosal-associated invariant T (MAIT) cells are unique innate-like T cells that are abundant in humans, accounting for 1-10% of circulating T cells and about 2% of total T cells in human oral cavity. MAIT cells can mount a strong immune response quickly without exogenous antigens and undergo a phenotypic transformation in the development of diseases. They produce cytokines involved in the Th1 and Th17 immune response and cytotoxic proteins, promote the dysfunction of autoreactive B cell and inhibit the function of NK cells. MAIT cells have been widely explored in autoimmune diseases, inflammatory diseases and tumors, and these mechanisms may also be involved in the pathogenesis of some oral diseases, while MAIT cells have not been systematically discussed in oral diseases. METHODS: We searched PubMed/MEDLINE, EMBASE and Microsoft Bing databases to review and analyze relevant literatures on the impact of MAIT cells in the pathogenesis of human oral diseases. CONCLUSION: Collected evidence elucidated the characteristics of MAIT cells and emphasized the potential roles of MAIT cells in oral lichen planus (OLP), chronic graft-versus-host disease (cGVHD), oral squamous cell carcinoma (OSCC), apical periodontitis (AP) and primary Sjogren's syndrome (pSS).

Alkannin reverses lipopolysaccharides-induced inflammatory responses by suppressing mitogen-activated protein kinase and nuclear factor kappa-B signalling.

Rheumatoid arthritis (RA) is an inflammatory disease that seriously affects human health worldwide. Meanwhile, inflammation in RAW264.7 cells could lead to the progression of RA. Alkannin (ALK) is derived from Alkanna tinctoria and is known to exert anti-tumor effects. However, the function of ALK in inflammation of RAW264.7 cells remains unclear. Thus, this research sought to investigate the detailed function of ALK in inflammatory responses of RAW264.7 cells. To induce an inflammatory response, RAW264.7 cells were exposed to lipopolysaccharide (LPS). MTT assay was applied to examine cell viability. Enzyme-linked immunosorbent assay (ELISA) was used to assess the levels of inflammatory cytokines. Furthermore, the mechanism underlying ALK function in inflammatory responses was investigated using RT-qPCR and western blotting. The data revealed that LPS significantly increased the expression of cyclooxygenase 2 (COX-2), Interleukin (IL)-1ß, inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and IL-6, whereas ALK reversed this effect. ALK also restored LPS-induced nuclear factor kappa-B (NF-κB) activation by inhibiting the downregulation of p-inhibitor kappa B alpha (IκBα). LPS elevated p-extracellular regulated protein kinases 1/2 (ERK1/2), phosphorylated p38 (p-p38), and phosphorylated -c-Jun N-terminal kinase (p-JNK) levels, which were markedly decreased in the presence of ALK. In summary, Alkannin attenuated LPS-induced inflammation by inhibiting NF-κB and MAPK signaling. Thus, our research might provide a new theoretical basis for exploring new strategies against RA.

Characterization and function of circulating mucosal-associated invariant T cells and γδT cells in oral lichen planus.

BACKGROUND: Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory disease with uncertain aetiology. Mucosal-associated invariant T (MAIT) cells and γδT cells are unconventional, innate-like T cells with immunoregulatory capacity. This study aimed to investigate the potential effects of MAIT and γδT cells on the pathogenesis of OLP. METHODS: Circulating MAIT cells and γδT cells were identified using flow cytometry. Surface proteins including CD4, CD8, CD69, CD103, CD49d, programmed death-1 (PD-1) and its ligand PD-L1 were assessed. Cytokines containing interleukin (IL)-4, IL-17, interferon (IFN)-γ, granzyme B and tumour necrosis factor (TNF)-α released by MAIT and γδT cells were measured following PMA and ionomycin stimulation. RESULTS: Circulating MAIT and γδT cells were deficient in OLP. The percentage of CD4+ , CD69+ , CD103+ and PD-1+ MAIT cells was increased in OLP, while that of CD8+ and CD49d+ MAIT cells was decreased. The percentage of CD103+ , PD-1+ and PD-L1+ γδT cells was upregulated in OLP. Both the MAIT and γδT cells in OLP produced less IL-4 than controls. The granzyme B-producing MAIT cells were increased, while γδT cells secreting granzyme B and TNF-α were reduced in OLP. IL-17 and IFN-γ in OLP MAIT and γδT cells were not significantly different from that in controls. The frequency of OLP MAIT cells and the MAIT/γδT rate were positively associated with the disease severity. CONCLUSION: The deficient MAIT and γδT cells expressing functional proteins and releasing cytokines may play an immunoregulatory role in the pathogenesis of OLP.

Evaluating Cancer-Related Biomarkers Based on Pathological Images: A Systematic Review.

Many diseases are accompanied by changes in certain biochemical indicators called biomarkers in cells or tissues. A variety of biomarkers, including proteins, nucleic acids, antibodies, and peptides, have been identified. Tumor biomarkers have been widely used in cancer risk assessment, early screening, diagnosis, prognosis, treatment, and progression monitoring. For example, the number of circulating tumor cell (CTC) is a prognostic indicator of breast cancer overall survival, and tumor mutation burden (TMB) can be used to predict the efficacy of immune checkpoint inhibitors. Currently, clinical methods such as polymerase chain reaction (PCR) and next generation sequencing (NGS) are mainly adopted to evaluate these biomarkers, which are time-consuming and expansive. Pathological image analysis is an essential tool in medical research, disease diagnosis and treatment, functioning by extracting important physiological and pathological information or knowledge from medical images. Recently, deep learning-based analysis on pathological images and morphology to predict tumor biomarkers has attracted great attention from both medical image and machine learning communities, as this combination not only reduces the burden on pathologists but also saves high costs and time. Therefore, it is necessary to summarize the current process of processing pathological images and key steps and methods used in each process, including: (1) pre-processing of pathological images, (2) image segmentation, (3) feature extraction, and (4) feature model construction. This will help people choose better and more appropriate medical image processing methods when predicting tumor biomarkers.

SKA3 promotes glioblastoma proliferation and invasion by enhancing the activation of Wnt/ß-catenin signaling via modulation of the Akt/GSK-3ß axis.

Spindle and kinetochore-related complex subunit 3 (SKA3) is a key modulator of the progression of multiple tumor types. However, the involvement of SKA3 in glioblastoma (GBM) has not been well studied. The current study aimed to explore the role of SKA3 expression and the potential function of the protein in GBM. Our data showed that SKA3 expression was significantly up-regulated in GBM. Functional assays demonstrated that the knockdown of SKA3 impeded the proliferation, colony formation and invasion of GBM cells, while SKA3 overexpression produced the opposite effects. Further investigation revealed that SKA3 overexpression enhanced the activation of Wnt/ß-catenin signaling, which was associated with the enhanced phosphorylation of Akt and glycogen synthase kinase-3ß (GSK-3ß). Notably, the inhibition of Akt markedly abrogated the SKA3 overexpression-induced promotion of Wnt/ß-catenin signaling in GBM cells. Further, the inhibition of Wnt/ß-catenin signaling markedly abrogated the SKA3 overexpression-induced promotion of tumor growth. In addition, the knockdown of SKA3 significantly retarded tumor formation and GBM progression in vivo. In summary, these data demonstrate that SKA3 exerts promotes tumor growth in GBM by enhancing the activation of Wnt/ß-catenin signaling via modulation of the Akt/GSK-3ß axis. This work highlights the pivotal role of SKA3/Akt/GSK-3ß/Wnt/ß-catenin signaling in the progression of GBM and suggests that SKA3 is an attractive therapeutic target with potential to be used to treat GBM.

Involvement of CD26 in Differentiation and Functions of Th1 and Th17 Subpopulations of T Lymphocytes.

CD26, acting as a costimulator of T cell activation, plays an important role in the immune system. However, the role of CD26 in the differentiation of T cell subsets, especially of new paradigms of T cells, such as Th17 and Tregs, is not fully clarified. In the present study, the role of CD26 in T cell differentiation was investigated in vitro. CD26 expression was analyzed in the different subsets of human peripheral blood T lymphocytes after solid-phase immobilized specific anti-CD3 mAb stimulation. Here, the percentage of CD4+ cells significantly increased and most of these cells were coexpressed with CD26, suggesting a close correlation of CD26 expression with the proliferation of CD4+ cells. Subsequently, after immobilized anti-CD3 mAb stimulation, CD26 high-expressing cells (CD26high) were separated from CD26 low-expressing cells (CD26low) by magnetic cell sorting. We found that the percentages of cells secreting Th1 typical cytokines (IL-2, IFN-γ) and Th17 typical cytokines (IL-6, IL-17, and IL-22) or expressing Th17 typical biomarkers (IL-23R, CD161, and CD196) in the CD26high group were markedly higher than in those in the CD26low group. In addition, a coexpression of CD26 with IL-2, IFN-γ, IL-17, IL-22, and IL-23R in lymphocytes was demonstrated by fluorescence microscopy. These results provide direct evidence that the high expression of CD26 is accompanied by the differentiation of T lymphocytes into Th1 and Th17, indicating that CD26 plays a crucial role in regulating the immune response.

LHPP exerts a tumor-inhibiting role in glioblastoma via the downregulation of Akt and Wnt/ß-catenin signaling.

Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) has been recently identified as a novel inhibitor of multiple tumors; however, its role in glioblastoma (GBM) has not been investigated. This study aimed to evaluate whether LHPP exerts a potential tumor-inhibiting role in GBM. Compared with that in normal tissues, LHPP expression was lower in GBM tissues and various GBM cell lines. LHPP up-regulation in GBM cells markedly reduced their proliferation and invasion, and its knockdown had an oncogenic effect on these cells. Further studies revealed that overexpressed LHPP decreased the levels of Akt and glycogen synthase-3ß phosphorylation and down-regulated Wnt/ß-catenin signaling. By contrast, LHPP knockdown produced opposite effects. Akt suppression markedly abrogated the activation of Wnt/ß-catenin signaling induced by LHPP knockdown. The reactivation of Wnt/ß-catenin signaling partially reversed the inhibition of tumor growth in GBM mediated by LHPP overexpression. In addition, LHPP overexpression markedly retarded the tumorigenesis of GBM cells in vivo. These findings revealed that LHPP acts a potential inhibitor of tumor growth in GBM, and its overexpression represses GBM proliferation and invasion by down-regulating Akt and Wnt/ß-catenin signaling. This work highlights the crucial role of LHPP in GBM progression and suggests its potential as an anticancer target for the treatment of this disease.

Omega-3 polyunsaturated fatty acids: a promising approach for the management of oral lichen planus.

BACKGROUND: Oral lichen planus (OLP) is a T-cell-mediated inflammatory disease with a risk of malignant transformation. Although the etiology of OLP is still uncertain, growing evidence suggests that oral microbiota, antigen-specific, and non-specific mechanisms are involved in the pathogenesis of OLP. Antigen-specific mechanisms include antigen presentation, T-cell activation, nuclear factor-kappa B signaling pathway, and cytokine secretion, while non-specific mechanisms consist of matrix metalloproteinases (MMP)-9 upregulation, psychological pressure, oxidative damage, aberrant expression of microRNAs (miRNAs), and autophagy. Till now, there is no cure for OLP, and the main purpose of OLP therapy is symptomatic control. FINDING: Seafood and its derivative omega-3 polyunsaturated fatty acids (n-3 PUFAs) can suppress antigen presentation, T-cell activation, and nuclear factor-kappa B signaling pathway, modulate the overexpressed inflammatory cytokines, inhibit the expression of MMP-9, as well as regulate the expression of miRNAs and autophagy. And they are possible agents for ameliorating psychological disorder and oxidative damage. Moreover, n-3 PUFAs supplementation has a beneficial effect on preventing tumorigenesis. CONCLUSION: n-3 PUFAs consumption may provide a non-toxic, inexpensive administration for OLP.

Emerging functions and clinical applications of exosomes in human oral diseases.

Exosomes are cell-derived membranous vesicles of endosomal origin secreted by all type of cells and present in various body fluids. Exosomes are enriched in peptides, lipids, and nucleic acids, emerging as vital modulators in intercellular communication. Exosomes are increasingly being evaluated as biomarkers for diagnosis and prognosis of diseases, because the constituents of exosomes could be reprogrammed depending on the states of diseases. These features also make exosomes a research hotspot in oral diseases in recent years. In this review, we outlined the characteristics of exosomes, focused on the differential expressions and altered biological functions of exosomes in oral diseases, including oral squamous cell carcinoma, oral leukoplakia, periodontitis, primary Sjögren's syndrome, oral lichen planus, as well as hand foot and mouth disease. Besides, accumulated evidence documents that it is implementable to consider the natural nanostructured exosomes as a new strategy for disease treatment. Herein, we highlighted the therapeutic potential of exosomes in oral tissue regeneration, oncotherapy, wound healing, and their superiority as therapeutic drug delivery vehicles.

Room temperature iron(ii)-catalyzed radical cyclization of unsaturated oximes with hypervalent iodine reagents.

Here, we disclose an iron(ii)-catalyzed I-O bond cleavage of Koser's hypervalent iodine reagents (HIRs) that initiated the radical cyclization of unsaturated oximes at room temperature. This strategy is successfully applied for the construction of the isoxazoline backbone in an efficient manner. In particular, the direct introduction of a TsO group into products facilitates their late-stage transformations in organic synthesis.

Black pepper and its bioactive constituent piperine: promising therapeutic strategies for oral lichen planus.

Oral lichen planus (OLP) is a common T cell-mediated chronic inflammatory disease with malignant potential and unclear etiology. The present study suggests that antigen-specific mechanisms in which dentritic cells, T lymphocytes and NF-κB signaling pathway play critical roles, are involved in the pathogenesis of OLP. Additionally, it has been indicated that altered expression of cyclooxygenase 2 (COX-2) and imbalanced oxidant-antioxidant status as well as psychological issue may act as promoters to the development of OLP. Therapies for OLP are primarily aimed to control symptoms and a specific cure is not yet available. Black pepper and its principle bioactive compound piperine have been reported to possess remarkable pharmacological activities. Not only has piperine been evidenced to exhibit repressive effects on the maturation of dentritic cells, the proliferation, activation and function of T lymphocytes as well as the NF-κB signaling pathway, but also to suppress the overproduction of COX-2 and weaken the oxidative stress. Furthermore, piperine might be a possible agent for alleviating psychological disorders and preventing carcinogenesis. Given all these into consideration, piperine may be a novel and effective therapeutic strategy for OLP.

Coexistence of IL-6 -572C/G and ICAM-1 K469E Polymorphisms among Patients with Sudden Sensorineural Hearing Loss.

Sudden sensorineural hearing loss (SSNHL) is a multifactorial disease, and its etiology remains elusive. SSNHL is possibly caused by both the environmental factors and genetic alterations. Recently, several studies suggested that inflammation may be involved in the pathogenesis of SSNHL, and certain gene polymorphisms may have correlations with SSNHL. Interleukin 6 (IL-6) functions both as a pro-inflammatory cytokine and an anti-inflammatory factor. Intercellular adhesion molecule-1 (ICAM-1) is a member of the immunoglobulin family that is also involved in inflammation response. Importantly, the IL-6 gene promoter contains a single nucleotide polymorphism (SNP), -572C/G, and ICAM-1 gene contains a SNP (A/G) in the protein-coding region, Lys (AAG)/Glu (GAG) at codon 469, known as K469E polymorphism. However, there is no study about the ICAM-1 gene polymorphism among SSNHL patients. In this study, we explored the relationship between SSNHL with IL-6 -572C/G and ICAM-1 K469E polymorphisms. We conducted a case-control study including 75 SSNHL patients and 165 healthy controls and analyzed the distribution and odds ratios of IL-6 and ICAM-1 genotypes. The frequency of the G allele at IL-6 -572C/G polymorphism was significantly higher among SSNHL patients than that among healthy individuals. In multivariate analysis, the coexistence of IL-6 -572G allele (GG/CG) and E allele (EE/KE) of ICAM-1 K469E polymorphism was significantly associated with an increased SSNHL risk (P < 0.001). In conclusion, we propose that the combination of IL-6 -572C/G and ICAM-1 K469E polymorphisms have a synergistic effect on the onset of SSNHL.

Degradable polyethylenimine derivate coupled to a bifunctional peptide R13 as a new gene-delivery vector.

BACKGROUND: To solve the efficiency versus cytotoxicity and tumor-targeting problems of polyethylenimine (PEI) used as a nonviral gene delivery vector, a degradable PEI derivate coupled to a bifunctional peptide R13 was developed. METHODS: First, we synthesized a degradable PEI derivate by crosslinking low-molecular-weight PEI with pluronic P123, then used tumor-targeting peptide arginine-glycine-aspartate-cysteine (RGDC), in conjunction with the cell-penetrating peptide Tat (49-57), to yield a bifunctional peptide RGDC-Tat (49-57) named R13, which can improve cell selection and increase cellular uptake, and, lastly, adopted R13 to modify the PEI derivates so as to prepare a new polymeric gene vector (P123-PEI-R13). The new gene vector was characterized in terms of its chemical structure and biophysical parameters. We also investigated the specificity, cytotoxicity, and gene transfection efficiency of this vector in αvß3-positive human cervical carcinoma Hela cells and murine melanoma B16 cells in vitro. RESULTS: The vector showed controlled degradation, strong targeting specificity to αvß3 receptor, and noncytotoxicity in Hela cells and B16 cells at higher doses, in contrast to PEI 25 KDa. The particle size of P123-PEI-R13/DNA complexes was around 100-250 nm, with proper zeta potential. The nanoparticles can protect plasmid DNA from being digested by DNase I at a concentration of 6 U DNase I/µg DNA. The nanoparticles were resistant to dissociation induced by 50% fetal bovine serum and 600 µg/mL sodium heparin. P123-PEI-R13 also revealed higher transfection efficiency in two cell lines as compared with PEI 25 KDa. CONCLUSION: P123-PEI-R13 is a potential candidate as a safe and efficient gene-delivery carrier for gene therapy.

Repressions of MMP-9 expression and NF-kappa B localization are involved in inhibition of lung carcinoma 95-D cell invasion by (-)-epigallocatechin-3-gallate.

Epigallocatechin-3-gallate (EGCG) repressed the invasion of lung carcinoma 95-D cells in invasion assay. RT-PCR analysis illuminated that 40 microM EGCG down-regulated the expression of MMP-9 by 45.7% and the result of Western blot analysis provided further evidence. NF-kappa B localized in the nucleus of the 95-D cells was diminished in a dose-dependent manner in EGCG-treated cells as shown by Western blot. Intracellular oxidants were more abundant in invasive cells than in invasion-suppressed cells fed with EGCG for 18 h. Thus, the inhibition of tumor invasion by EGCG was shown to be attributed to decreases of the expression of MMP-9 and NF-kappa B, which may result from decrease of intracellular oxidants.