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Dual-targeting SERS-encoded graphene oxide nanocarrier with regard to intracellular co-delivery of doxorubicin as well as 9-aminoacridine using improved blend remedy.
The colorectal tumor-derived exosomes activated HSCs to secrete excessive IL-6. Furthermore, the conditioned medium of activated HSCs enhanced the lactate metabolism of hypoxic tumor cells by activating the IL-6/STAT3 pathway and upregulating the downstream MCT1 and LDHB, in order to confer the resistance of SN38, which is the active metabolite of irinotecan.

Taken together, the cultured supernatant of normoxic exosome-educated HSCs enhances the lactate metabolism of hypoxic tumor cells via the IL-6/STAT3 pathway, in order to confer the SN38 resistance in a mimic liver metastatic microenvironment.
Taken together, the cultured supernatant of normoxic exosome-educated HSCs enhances the lactate metabolism of hypoxic tumor cells via the IL-6/STAT3 pathway, in order to confer the SN38 resistance in a mimic liver metastatic microenvironment.
To investigate the characteristics of hematological malignancies in patients with the
fusion gene and provide a literature review.

We retrospectively analyzed the clinical data of three cases of acute leukemia and myeloid neoplasms harboring the
fusion gene who were treated at our hospital. Their clinical manifestations, pathological results and treatment strategies were investigated.

The three cases were diagnosed with T-cell acute lymphoblastic leukemia (T-ALL), acute myeloid leukemia (AML) and myeloid sarcoma (MS), respectively. Karyotype analyses identified a normal result in all three patients. Subsequently, we confirmed del(9q34) utilizing FISH analysis. Mutation of the
gene was detected in case 1, while mutations in
and
were detected in case 2, which have not been officially reported in patients with
fusions. Finally, relevant literature focusing on adult patients with hematological malignancies harboring the
fusion gene were summarized.

Adult patients with the
fusion gene were rare among cases of hematological malignancies. There was a large degree of heterogeneity between different patients. Notably, some patients remained sensitive to chemotherapy. Overall prognosis may be related to the type of disease and other cytogenetic abnormalities. Systemic cytogenetic and molecular studies are needed to make accurate diagnoses. Additional cases need to be accumulated and summarized to better understand these diseases.
Adult patients with the SET-CAN fusion gene were rare among cases of hematological malignancies. There was a large degree of heterogeneity between different patients. Notably, some patients remained sensitive to chemotherapy. Overall prognosis may be related to the type of disease and other cytogenetic abnormalities. Systemic cytogenetic and molecular studies are needed to make accurate diagnoses. Additional cases need to be accumulated and summarized to better understand these diseases.
Prostate cancer is one of the most common malignancies in urology, especially in developed countries. Our previous studies showed that Lanthionine synthase C-like protein 1 (
) can promote the proliferation of prostate cancer cells and protect cells from oxidative stress. Also,
protects cells by inhibiting the
signaling pathway after H
O
treatment.

In our study, we analyzed the data of RNA-seq to identify the DEGs after
overexpression. We performed a functional enrichment analysis with gene set enrichment analysis (GSEA) and a database for annotation, visualization, and integrated discovery (DAVID). We also identified the critical hub gene correlated with disease prognosis by Cox regression analysis.

A total of 8928 DEGs were identified. Through the analysis of GO and KEGG, we found that DEGs are significantly enriched in categories related to metabolism, cancer-related signaling pathways, and inflammation. The top 15 hub genes were then identified and ranked by degree from the protein-protein interaction network. Survival analysis showed 4 hub genes related to disease prognosis and
expression is an independent risk factor for the prognosis.

Our results suggest the critical genes and pathways that might play key roles after
overexpression in prostate cancer. We also provide candidate gene targets that might play important roles in prostate cancer development.
Our results suggest the critical genes and pathways that might play key roles after LanCL1 overexpression in prostate cancer. We also provide candidate gene targets that might play important roles in prostate cancer development.
Colorectal cancer (CRC), the third most common cancer worldwide, involves a physiological and pathological long non-coding RNA (lncRNA) paradigm shift. It has been reported that the lncRNA LOXL1-AS1 affects tumor development for many kinds of cancers, but its functions and mechanisms in CRC remain unknown.

Expression levels of LOXL1-AS1 and miR-708-5p within CRC tissues and cell lines were measured using qRT-PCR. The performance of gain-of-function and loss-of-function assays was aimed at examining the effects of LOXL1-AS1 and miR-708-5p; colony formation and cell viability assays were carried out to measure cell multiplication; and Transwell migration and wound-healing assays were carried out for the measurement of cell migration and invasion. Luciferase reporter assay was used to verify the interactions between LOXL1-AS1 and miR-708-5p and between miR-708-5p and the CD44-EGFR signaling pathway. Finally, expression of CD44 and EGFR proteins was measured by Western blot and immunofluorescence assays.

In this study, we reveal that the regulation of lncRNA LOXL1-AS1 occurs within CRC based on the correlation with poor clinical outcomes. LOXL1-AS1 knockdown along with miR-708-5p overpresentation in CRC cell lines inhibited cell multiplication, migration, and invasion. The inhibiting effect of LOXL1-AS1 knockdown on CRC was reversed by upregulating the CD44-EGFR signal pathway. From the perspective of mechanism, LOXL1-AS1 imposes sponging upon miR-708-5p and thereby promotes the CD44-EGFR signal pathway in CRC cells.

This study demonstrated that lncRNA LOXL1-AS1 enhances multiplication, migration, invasion, and progression of CRC by sponging miR-708-5p to regulate the CD44-EGFR signal pathway.
This study demonstrated that lncRNA LOXL1-AS1 enhances multiplication, migration, invasion, and progression of CRC by sponging miR-708-5p to regulate the CD44-EGFR signal pathway.
Although gefitinib brings about tremendous advances in the treatment of non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations, most of patients become incurable due to drug resistance. JuBei oral liquid (JB) has been widely used to treat pneumonia in clinic. Components of JB were reported to induce apoptosis in NSCLC, which indicated that JB could be a potential antitumor agent for NSCLC patients. In this study, we investigated the effect of JB on gefitinib-sensitive PC-9 and gefitinib-resistant PC-9/GR, H1975 cells as well as its underlying molecular mechanisms.

PC-9, PC-9/GR and H1975 cells were treated with JB, LY294002, SCH772984, gefitinib alone or in combination. Then, cell viability, colony formation, cell death, expression of mitochondria-dependent pathway proteins, expression of EGFR, PI3K/AKT, MAPK signal pathway proteins, Bcl-2 mitochondrial translocation, ROS generation and cell apoptosis were examined by MTT, colony forming, live/dead cell staining, We indicated that JB could be a potential therapeutic agent for NSCLC patients harboring EGFR mutations as well as those under gefitinib resistance.
Long-noncoding RNAs (lncRNAs) could exert a crucial effect on the development of human cancers, including CRC. However, the biological function and underlying mechanism of
in the development of CRC still need deeper exploration.

The expression of
in CRC tissues and cell lines was assessed by qRT-PCR. Cell proliferation, migration, and invasion were measured by the respective cell counting Kit-8 (CCK-8), wound healing assay and transwell invasion assay. Cell apoptosis and caspase-3 activity were detected by flow cytometry and caspase-3 activity assay. The relationship between LINC00460 and miR-613 expression was explored by Dual-luciferase reporter assay. Protein expression was measured by Western blotting. In vivo tumour growth was evaluated using a xenograft model of nude mice.

LINC00460 was markedly up-regulated in CRC tissues and cell lines compared to their corresponding controls, which was closely correlated with clinical stage, TNM (T) classification, nodal (N) classification, metastasis (M)nts.
LINC00460 functions as a competing endogenous RNA to regulate SphK1 expression by sponging miR-613 in CRC and provides a valuable therapeutic strategy for CRC patients.
Tumor-associated macrophages (TAMs) originate from monocytes and differentiate into mature macrophages. The interaction between cancer cells and TAMs promotes tumor growth and suppresses immunosurveillance. However, this phenomenon has seldom been observed in ampullary cancer.

TAMs in ampullary cancer were investigated using immunohistochemical (IHC) staining of cancer tissues. Bioinformatic analysis of data from the Gene Expression Omnibus (GEO) database revealed transforming growth factor-beta (TGF-β) signaling in ampullary cancer. The complementary DNA microarray of cancer was compared with adjacent normal duodenum and enzyme-linked immunosorbent assay of serum was used to verify TGF-β signaling in patients. The THP-1 cell line was activated

to imitate M2 TAMs. learn more ClueGo and CluePedia software were operated to simulate TGF-β-related networks in ampullary cancer.

The IHC study revealed that the majority of TAMs inside ampullary cancer were cluster of differentiation (CD)163
cells and that the expression of mature CD68
macrophages was correlated with advanced cancer stage. Bioinformatics analysis revealed that TGF-β and its downstream signaling were significantly upregulated. To verify our bioinformatics-derived predictions, we performed several experiments and demonstrated that increased TGF-β expression was detected in the cDNA microarray. Higher serum levels of TGF-β were correlated with fewer CD68
and more inducible nitric oxide synthase macrophages in ampullary cancer. Treatment with TGF-β induced modulation of THP-1-derived macrophages.

The present study demonstrates that TGF-β modulates macrophage activity in ampullary cancer. Targeting TGF-β could be an approach to activating immunosurveillance.
The present study demonstrates that TGF-β modulates macrophage activity in ampullary cancer. Targeting TGF-β could be an approach to activating immunosurveillance.
Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Increasing evidence showed that circular RNAs (circRNAs) played critical roles in the progression of CRC. However, the effects and underlying mechanisms of circ_0000512 in CRC progression remain unclear.

The expression levels of circ_0000512, microRNA-296-5p (miR-296-5p) and runt-related transcription factor 1 (RUNX1) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, colony formation, cell cycle distribution and cell apoptosis were detected by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and flow cytometry analysis, respectively. Western blot assay was utilized to measure the protein expression of Cyclin D1, Cleaved Caspase-3 and RUNX1. The interaction between miR-296-5p and circ_0000512 or RUNX1 was predicted by starBase and verified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. The mice xenograft model was established to explore the function of circ_0000512 in vivo.
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