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Serum response factor (SRF), a sequence-specific transcription factor, is closely related to metastasis of gastric cancer, a digestive tract cancer. Herein, we probed the effect of SRF on metastasis and progression of colon cancer (CC), another digestive tract disorder, and the detailed mechanism.
Microarray analysis was conducted on tumor and adjacent tissues to filter differentially expressed miRNA, followed by RT-qPCR validation in CC cell lines. The transcription factor and the target gene of microRNA-214 (miR-214) were predicted, and their binding relationships were tested by luciferase reporter assays and ChIP assays. Subsequently, SRF and protein tyrosine kinase 6 (PTK6) expression in CC patients and cells was evaluated by RT-qPCR, while JAK2 and STAT3 expression in cells by Western blot analysis. To further explore functions of miR-214, PTK6 and SRF on CC, CC cells were delivered with si-PTK6, miR-214 mimic and/or SRF overexpression.
miR-214 expressed poorly in CC tissues and cell lines, which related to advanced TNM staging and survival. miR-214 mimic inhibited proliferation, migration, invasion, xenograft tumor growth and metastasis of CC cells. SRF, overexpressed in CC samples and cells, suppressed the transcription of miR-214. Meanwhile, SRF upregulation counteracted the inhibitory role of miR-214 mimic in CC cell growth. miR-214 negatively regulated PTK6 expression to impair the JAK2/STAT3 pathway activation, thereby halting CC cell proliferation, migration, invasion, xenograft tumor growth and metastasis.
Altogether, miR-214 may perform as a tumor suppressor in CC, and the SRF/miR-214/PTK6/JAK2/STAT3 axis could be applied as a biomarker and potential therapeutic target.
Altogether, miR-214 may perform as a tumor suppressor in CC, and the SRF/miR-214/PTK6/JAK2/STAT3 axis could be applied as a biomarker and potential therapeutic target.The outbreak of the COVID-19 is currently the biggest international concern. Treatment of gastric cancer (GC) patients in the pandemic era with high hospital burden and under severe oncological/surgical resource constraints should implicate a need for resource re-allocation with a new "pandemic" GC treatment algorithm. The neoadjuvant/perioperative (radio-)chemotherapy is applied in the majority of advanced GC cases with poor postoperative therapy compliance. In the East, radical surgery is frequently used in the first instance, with adjuvant chemotherapy reserved for patients with a high risk of recurrence. Moreover, the elderly population might be effectively treated by surgery alone, thus saving oncological resources for younger people who need a more aggressive approach. In this framework, prioritization is a key concept based on the severity of symptoms and the need for urgent (surgical) intervention. High-risk and marginally effective surgery should be replaced with definitive radio- and/or chemotherapy. The pandemic framework to provide optimal care for GC patients must be based on multidisciplinary decision-making and include all anti-cancer treatment options surgery, systemic therapy, and radiotherapy. Sulbactam pivoxil research buy The priority and staffing dictate adherence to the new algorithm. We believe that these priorities may improve the delivery of care to all, including elderly GC patients.
The clinical implications of the metabolic parameters of
F-fluorodeoxyglucose positron emission tomography-computed tomography (
F-FDG PET/CT) in epidermal growth factor receptor (
-mutated lung cancer are not fully understood. The aim of this study was to evaluate the diagnostic and prognostic utility of the parameters in
-mutated lung cancer patients.
We retrospectively enrolled 134 patients with advanced lung adenocarcinoma (72
-negative and 62
positive). We evaluated the correlation between
mutational status and the maximum standardized uptake value (SUVmax), as well as the associations between treatment outcomes in
-mutated patients and various metabolic parameters of primary tumors. For the best predictive parameters, we calculated the metabolic tumor volume (MTV) and total lesion glycolysis (TLG) using two SUV cutoffs 1.5 (MTV
, TLG
) and 2.5 (MTV
, TLG
).
Mean SUVmax was lower for
-mutated tumors compared with
wild-type (6.11 vs 10.41,
< 0.001) tumors. Low SUVmax was significantly associated with positive
mutation (odds ratio = 1.74). Multivariate analysis for survival demonstrated that high MTV
, TLG
, MTV
, and TLG
were independently associated with shorter progression-free survival (PFS) and overall survival (OS), and the highest hazard ratios were found in TLG
(3.26 for PFS and 4.62 for OS).
SUVmax may be predictive for
mutational status, and MTV and TLG of primary tumors may be promising prognostic parameters;
F-FDG PET/CT has potential utility for the risk stratification of
-mutated patients treated with targeted therapy.
SUVmax may be predictive for EGFR mutational status, and MTV and TLG of primary tumors may be promising prognostic parameters; 18F-FDG PET/CT has potential utility for the risk stratification of EGFR-mutated patients treated with targeted therapy.
As a malignant tumor, the progression of osteosarcoma (OS) is mediated by multiple regulators, including circular RNAs (circRNAs). However, the role of circ_0000885 in OS is unclear.
Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of circ_0000885, miR-1294 and fibroblast growth factor receptor 1 (FGFR1). Cell proliferation was evaluated using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Flow cytometry and transwell assay were employed to determine the cell cycle distribution, cell migration and invasion, respectively. Moreover, the relationship between miR-1294 and circ_0000885 or FGFR1 was confirmed by dual-luciferase reporter assay. The protein level of FGFR1 was assessed via Western blot (WB) analysis. Animal experiments were used to verify the effect of circ_0000885 silencing on OS tumor growth in vivo.
Circ_0000885 level was increased in OS tissues and cells. Knockdown of circ_0000885 repressed the proliferation, migration, invasion and induced cell cycle arrest in OS cells.