Notes

Comprehending the physiology of the medical malpractice fit. In the United States this is the physician's best defense.
Purpose To investigate the role of EGFR and STAT3 in breast cancer development and progression. Methods Through bioinformatics analysis differently expressed genes (DEGs) including EGFR and STAT3 were identified in breast cancer tissue. QRT-PCR and Western blot analysis were used to investigate EGFR and STAT3 levels in breast cancer tissues and cells. The influence of EGFR and STAT3 on the breast cancer cell proliferation (CCK-8 assay, clone formation assays), migration (wound healing assays) and invasion (transwell assays) were investigated. The influence of EGFR on breast cancer in vivo was examined by Nude mouse transplantation tumor experiments and immunohistochemistry (IHC) staining. The effects of EGFR on breast cancer signaling were assessed via Western blot. Results Both EGFR and p-STAT3 were up-regulated in breast cancer tissues and cell lines. EGFR expression was positively associated with p-STAT3. Moreover, EGFR and p-STAT3 activity enhanced the proliferation and invasion of tumor cells. Breast cancer cell growth was dramatically inhibited by EGFR silencing in vivo. Conclusion EGFR promotes breast cancer progression via STAT3 phosphorylation and JAK/STAT3 signaling. © 2020 Song et al.Berberine (BBR) has been extensively studied in vivo and vitro experiments. BBR inhibits cell proliferation by regulating cell cycle and cell autophagy, and promoting cell apoptosis. BBR also inhibits cell invasion and metastasis by suppressing EMT and down-regulating the expression of metastasis-related proteins and signaling pathways. In addition, BBR inhibits cell proliferation by interacting with microRNAs and suppressing telomerase activity. BBR exerts its anti-inflammation and antioxidant properties, and also regulates tumor microenvironment. This review emphasized that BBR as a potential anti-inflammation and antioxidant agent, also as an effective immunomodulator, is expected to be widely used in clinic for cancer therapy. © 2020 Wang et al.Background Growing evidence indicates that long noncoding RNA (lncRNA) is a group of important regulator in cancer development. However, the correlation between lncRNA and ovarian cancer remains elusive. Here, we aimed to investigate the roles of LEF1-AS1 in ovarian cancer progression. Methods LEF1-AS1 expression was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Survival rate was analyzed by Kaplan-Meier method. Cell Counting Kit-8 (CCK8) and colony formation assays were used for proliferation analysis. Transwell assay was utilized for analyses of migration and invasion. Luciferase reporter assay was performed to test the interaction between LEF1-AS1 and miR-1285-3p. Results We showed that LEF1-AS1 expression was upregulated in ovarian cancer tissues compared with normal tissues. Besides, LEF1-AS1 level was positively correlated with lymph node metastasis and advanced stage. Enhanced expression of LEF1-AS1 may predict a poor prognosis. Moreover, LEF1-AS1 knockdown suppressed ovarian cancer cell proliferation, migration and invasion. Selleckchem RP-3500 Mechanistically, LEF1-AS1 exerted its oncogenic functions through interacting with miR-1285-3p to inhibit miRNA activity. Rescue assay validated that miR-1285-3p inhibitors abrogated LEF1-AS1-silencer-caused suppression of ovarian cancer progression. Conclusion Our study revealed that LEF1-AS1 acts as a vital regulation in ovarian cancer progression. © 2020 Zhang and Ruan.Neoadjuvant hormonal therapy (NEO-HT) is a possible treatment option for breast cancer (BC) patient with estrogen receptor positive (ER+) and HER2 negative (HER2-) disease. The absence of solid data on the type of drugs to be used and duration of treatment as well as lack of clear evidence of effectiveness of NEO-HT compared to chemotherapy (CT) reserve its use for patients with old age or frail conditions. However, the low pathologic complete response rate (pCR) obtained with tamoxifen or aromatase inhibitors (AIs) alone does not make NEO-HT as a suitable option for the neoadjuvant treatment of HR+ HER2-. The use of the cyclin-dependent kinase 4 and 6 (CDK 4/6) inhibitors palbociclib, ribociclib and abemaciclib of the mammalian target of rapamycin (mTOR) inhibitor everolimus and of the phosphoinositide 3 kinase (PI3K) inhibitor taselisib together with endocrine therapy (ET) has become a standard in advanced breast cancer, showing clinical effectiveness and significantly prolonging median progression-free survival compared to ET only. In the early phase disease, the use of ET together with CDK 4/6, mTOR and PI3K inhibitors is still investigational. Data from recent studies are promising even though less impressive than in metastatic setting. In this context, the use of genomic-transcriptomic tools (such as ONCOTYPE, PAM50) and the identification of novel biomarkers (ESR1, PI3Kca, PDGF-R) on tissue or with liquid biopsy could help to select patient prone to respond to endocrine-combined therapy and able to achieve pCR. With our review, we aimed at evaluating the current state of the art in the treatment of locally advanced breast cancer with NEO-HT. © 2020 Grizzi et al.Background The microtubule actin cross-linking factor 1 (MACF1) is involved in cellular migration, adhesion, and invasion processes. Its abnormal expression initiates tumor cell proliferation and metastasis in numerous cancer types. Methods In this study, we utilized short hair-pin RNA interference of MACF1 to assess the inhibitory effects on the metastatic potential of B16F10 melanoma cells both in vitro and in vivo a mouse model. Results The MACF1 expression was increased in B16F10 cells-induced tumor tissues; while the down-regulation of MACF1 impacted the B16F10 melanoma cell metastatic behavior by decreasing the ability of colony formation and invasion in vitro as well as inhibiting B16F10 cells-induced tumor growth and lung metastasis in vivo. The results of Western blot and immunohistochemistry indicated that the expression of E-cadherin and Smad-7 was significantly increased whereas the expression of N-cadherin and TGF-β1 was significantly decreased in tumor tissue of mice challenged with the B16F10/MACF1-RNAi cells when compared with the B16F10 cells challenged mice. Conclusion The data presented in this study demonstrated that down-regulated MACF1 expression decreased B16F10 melanoma metastasis in mice by inhibiting the epithelial to mesenchymal transition program. Thus, MACF1 may be a novel target for melanoma therapy. © 2020 Wang et al.Purpose Ovarian cancer is the most lethal of gynecological malignancies. Dihydroartemisinin (DHA), a derivative of artemisinin (ARS), has profound effects against human tumors. The aim of this study was to provide a convenient, cost-efficient technique, Fourier transform infrared (FTIR) spectroscopy, to monitor and evaluate responses to DHA-induced growth inhibition of ovarian cancer cells. Methods Cell growth and viability and the 50% inhibitory concentration (IC50) of DHA were assessed by the MTT assay. FTIR spectroscopy was used to monitor cells following DHA treatment, and data were analyzed by OMNIC 8.0 software. Results DHA can decrease the viability of ovarian cancer cells and normal cells, but cancer cells were more sensitive to this drug than normal cells. Spectral differences were observed between cells with or without DHA treatment. In particular, an increase in the amount of lipids and nucleic acids was observed. The band intensity ratio of 1454/1400, and the intensity of the band 1741 cm-1 increased, indicating stronger absorption after DHA treatment. Moreover, the differences were larger for the cell lines that were more sensitive to DHA. Conclusion The spectral features provided information about important molecular characteristics of the cells in response to chemicals. These findings demonstrated the possible use of FTIR spectroscopy to evaluate DHA-induced growth inhibition effects in ovarian cancer cells and provided a promising new tool for monitoring cell growth and the effects of antitumor drugs in the clinic in the future. © 2020 Li et al.Purpose Paeonol, a natural product derived from the root of Cynanchum paniculatum (Bunge) K. Schum and the root of Paeonia suffruticosa Andr. (Ranunculaceae) has attracted extensive attention for its anti-cancer proliferation effect in recent years. The present study examined the role of paeonol in suppressing migration and invasion in pancreatic cancer cells by inhibiting TGF-β1/Smad signaling. Methods Cell viability was evaluated by MTT and colonial formation assay. Migration and invasion capabilities were examined by cell scratch-wound healing assay and the Boyden chamber invasion assay. Western Blot and qRT-PCR were used to measure the protein and RNA levels of vimentin, E-cadherin, N-cadherin, and TGF-β1/Smad signaling. Results At non-cytotoxic dose, 100 μΜ and 150 μΜ of paeonol showed significant anti-migration and anti-invasion effects on Panc-1 and Capan-1 cells (p less then 0.01). Paeonol inhibited epithelial-mesenchymal-transition by upregulating E-cadherin, and down regulating N-cadherin and vimentin expressions. Paeonol inhibited TGF-β1/Smad signaling pathway by downregulating TGF-β1, p-Smad2/Smad2 and p-Smad3/Smad3 expressions. Further, TGF-β1 attenuated the anti-migration and anti-invasion capacities of paeonol in Panc-1 and Capan-1 cells. Conclusion These findings revealed that paeonol could suppress proliferation and inhibit migration and invasion in Panc-1 and Capan-1 cells by inhibiting the TGF-β1/Smad pathway and might be a promising novel anti-pancreatic cancer drug. © 2020 Cheng et al.Background A new regulatory subpopulation of ILCs, ILCreg has been identified in mouse and human intestines. ILCregs share characteristics with both innate lymphoid cells and regulatory cells; however, the significance of CD45+Lin-CD127+IL-10+ ILCregs in patients with AML remains unclear. Intriguingly, ILCregs constitutively express id2, id3, sox4, tgfbr1, tgfbr2, il2rb and il2rg, but the significance of miRNAs associated with these genes has yet to be explored. In this study, we evaluate ILCreg frequency, ILCreg gene-associated miRNA quantification, and its significance in patients with AML and normal donors. Methods Using 4 color combinations of surface and intracellular antibody staining, the CD45+Lin-CD127+IL-10+ ILCregs from 12 normal donors and 42 patients newly diagnosed with AML were measured by flow cytometry. Plasma samples and bone marrow cells from 6 normal donors and 9 patients with AML were studied by next-generation sequence miRNAs quantification. Results Our results showed that the frequency oficant difference between AML patients and normal donors (both Q and P-value less then 0.001). Among them, 4 miRNAs (hsa-miR-193b-3p, hsa-miR-1270, hsa-miR-210-3p, and hsa-miR-486-3p) were detected in both plasma and BM cell samples. link2 Conclusion Our study enumerated ILCregs, then measured miRNAs from those ILCregs in AML samples for the first time. The results demonstrated the deficiency of ILCreg and differential expression of miRNAs in patients with AML. © 2019 Yu et al.Introduction Hepatocellular carcinoma (HCC) is one of the most common malignant cancers, while the molecular mechanism is not clear. link3 Circular RNAs (circRNAs) are a class of naturally occurring endogenous noncoding RNAs that prove to play important roles in the occurrence, development and prognosis of HCC. In this study, we focused on an abnormally expressed circular RNA-circPCNX in HCC and study the function of circPCNX and Pecanex (PCNX) in HCC. Methods Circular RNA sequencing was used to find the abnormally expressed circRNAs and qRT-PCR was used to verify it. CCK8 assay, colony formation assay and cell apoptosis assay were used to study biological functions, and Luciferase reporter assay and Western blot analysis were used to study the mechanism. Results We observed that circPCNX and Pecanex were significantly upregulated in tumor tissues of patients with HCC and correlated with clinicopathological variables or prognosis of HCC patients. Functional investigations showed circPCNX and Pecanex could promote the viability of HCC cells.
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