Koefoedsong2415
s excluding breast cancer and toxicities could be well controlled. MK-0859 The study is a pilot study motivating larger studies to elucidate the safety and efficacy of pyrotinib in non-breast solid tumors.
Incidental gallbladder cancer (IGBC) is defined as gallbladder cancer (GBC) that is accidentally discovered during cholecystectomy to treat benign lesions. We aimed to compare the prognosis of IGBC patients who underwent simultaneous radical resection (SIR) vs salvage radical resection (SAR).
We retrospectively reviewed data for IGBC patients admitted to Sir Run Run Shaw Hospital from January 2000 to May 2016. Survival analysis was performed using Kaplan-Meier (univariate) and COX regression (multivariate) analyses.
Eighty-four patients with IGBC underwent radical resection; 43/84 underwent SIR, and 41/84 underwent SAR. Compared with SIR, the SAR group was more likely to receive comprehensive preoperative radiographic evaluation, port-site excision, and have more lymph nodes excised (all P < 0.05). Kaplan-Meier analysis indicated that the prognosis in the SAR group was better than that in SIR (overall survival P = 0.050, recurrence-free survival P = 0.028). Regression analysis indicated that the type of radical resection (SIR/SAR) was not an independent prognostic factor (overall survival P = 0.737, recurrence-free survival P = 0.957).
Patients undergoing SAR had non-inferior survival compared with SIR. It is possible that patients in SAR underwent preoperative radiographical evaluations more comprehensively and the surgical operations were more well performed.
Patients undergoing SAR had non-inferior survival compared with SIR. It is possible that patients in SAR underwent preoperative radiographical evaluations more comprehensively and the surgical operations were more well performed.
lncRNA has been proven to be oncogenic in a variety of cancers, but its role in other types of cancer remains unclear. This study was to investigate the role of
in retinoblastoma (Rb).
RT-qPCR was performed to determine the expression of
and miR34a in paired Rb and nontumor tissue. Overexpression of
and miR34a in Rb cells was achieved to evaluate the interaction between them. Methylation-specific PCR was used to analyze the effect of
overexpression on
gene methylation. CCK8 assays were used to analyze cell proliferation.
The results showed that
expression was upregulated and miR34a expression downregulated in Rb tissue. Moreover, miR34a expression was negatively correlated with the of
expression in Rb tissue. Overexpression of
decreased expression of miR34a and increased methylation of
in Rb cells. In addition, overexpression of
reduced the inhibitory effects of miR34a on Rb-cell proliferation.
may promote Rb cell proliferation by downregulating miR34a methylation.
CASC8 may promote Rb cell proliferation by downregulating miR34a methylation.
RUNX1-IT1 suppresses colorectal cancer and liver cancer, while its role in other cancers is unknown. This study was performed to investigate the role of RUNX1-IT1 in endometrial cancer (EC).
EC and paired non-tumor tissues were collected from 62 EC patients, and the expression of RUNX1-IT1, mature miR-21 and miR-21 precursor in these tissue samples were determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of RUNX1-IT1 was achieved in EC cells and the expression of mature miR-21 and miR-21 precursor were analyzed by RT-qPCR. CCK-8 assay was used for cell proliferation analysis.
We found that RUNX1-IT1 was downregulated in EC and inversely correlated with mature miR-21 but not miR-21 precursor. RUNX1-IT1 was predicted to bind with miR-21 precursor. The interaction between them was verified by dual-luciferase activity assay and RNA pull-down assay. In EC cells, overexpression of RUNX1-IT1 downregulated mature miR-21, but not miR-21 precursor. Overexpression of RUNX1-IT1 suppressed the role of miR-21 in increasing cell proliferation.
RUNX1-IT1 is downregulated in EC and inhibits cancer cell proliferation by suppressing the maturation of miR-21.
RUNX1-IT1 is downregulated in EC and inhibits cancer cell proliferation by suppressing the maturation of miR-21.
Renal cell carcinoma (RCC) is one of the most common malignancies globally, among which clear cell carcinoma (ccRCC) accounts for 85-90% of all pathological types. This study aims to screen out potential genes in metastatic ccRCC so as to provide novel insights for ccRCC treatment.
GSE53757 and GSE84546 datasets in the Gene Expression Omnibus (GEO) were profiled to identify differentially expressed genes (DEGs) from ccRCC samples with or without metastasis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and the gene ontology (GO) analysis were performed to analyze pathway enrichment and functional annotation of DEGs. Protein-protein interaction (PPI) network was constructed, and survival analysis was conducted to evaluate the clinical values of the identified hub genes. In vitro loss-of-function assays were performed to explore the biological roles of these genes.
The bioinformatic analysis indicated that 312 DEGs were identified, including 148 upregulated genes and 164 downregulated ones. Using PPI and Cytoscape, 10 hub genes were selected (
,
,
,
,
,
,
,
,
, and
) from DEGs which might be closely related with ccRCC metastasis. In Kaplan-Meier analysis, three potential prognostic biomarkers (
,
and
) were identified. Finally, cell proliferative and invasive assays further verified that
,
and
were associated with the proliferation and invasion of ccRCC cells.
Our results demonstrated that metastatic ccRCC was partially attributed to the aberrant expression of
,
and
, and more personalized therapeutic approaches should be explored targeting these hub genes.
Our results demonstrated that metastatic ccRCC was partially attributed to the aberrant expression of KIF20A, CCNB2 and CDCA8, and more personalized therapeutic approaches should be explored targeting these hub genes.
The acquisition of chemoresistance to methotrexate (MTX) still remains one of the major challenges for choriocarcinoma treatment. Herein, we aimed to evaluate the potential role of Signaling Lymphocytic Activation Molecule Family Member 1 (SLAMF1) as a possible regulator of chemoresistance to MTX in choriocarcinoma.
MTX-resistant JEG3 and JAR sublines (JEG3/MTX, JAR/MTX) were used to study SLAMF1 function. CCK8 assay and soft agar assay were conducted to measure the cell viability and clonogenesis of choriocarcinoma cells, respectively; MDC incorporation assay was conducted for the quantification of intracellular autophagy; BrdU labeling was used to assess the proliferative potential of choriocarcinoma cells; SLAMF1 protein expression was analyzed by Western blotting.
Upregulation of SLAMF1 expression was observed in MTX-resistant JEG3/MTX and JAR/MTX sublines compared to their parental JEG3 and JAR cell lines, respectively. Knockdown of SLAMF1 markedly attenuated cell viability and soft agar clonogenesis after incubation with MTX in JEG3/MTX and JAR/MTX cells.
