Notes

Bioindicator reptile displays genomic signatures associated with normal and also anthropogenic barriers to gene circulation.
Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice.

Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.
Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.
Although the survival rate of colorectal cancer (CRC) patients can be improved by surgery, radiotherapy, and chemotherapy, the resistance to 5-fluorouracil (5-Fu) affects the effect of chemotherapy and the prognosis of patients. An increasing number of studies showed that 5-Fu resistance was the main reason for the failure of colorectal cancer treatment. The poor prognosis of colorectal cancer greatly harms people's health. This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance.

Cell proliferation and invasion experiments showed that down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Tumor growth was inhibited by down-regulation of CDK1 in tumor xenograft mouse models.

We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. We also confirmed that the differential expression of 5-Fu in tumor tissues was related to tumor site, lymph node metastasis and stage. CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo.

High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.
High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.
5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) is an effective chemotherapy for colorectal cancer (CRC) in clinic. Deruxtecan It remains unclear regarding the effect of circular RNA (circRNA) circ_0032833 on regulating chemosensitivity in CRC.

Drug resistance analysis was performed by Cell Counting Kit-8 (CCK-8) assay. All RNA and protein levels were, respectively, measured via quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Cellular colony capacity, apoptosis and metastasis were evaluated using colony formation assay, Annexin-FITC/PI flow cytometry and transwell migration/invasion assays. The molecular combination was notarized using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The in vivo experiment was conducted via xenograft tumors in mice.

Circ_0032833 was significantly up-regulated in FOLFOX-resistant CRC and associated with drug resistance. Knockdown of circ_0032833 could sensitize FOLFOX-resistant CRC cells to 5-fluorouracil and oxaliplatin. Circ_003d developing a novel strategy to enhance chemosensitivity in CRC.
Breast cancer (BC) remains the most common malignancy among women. Circular RNAs (circRNAs) have been demonstrated to play important roles in human cancers, including BC. In this study, we sought to identify the precise parts of circ_0061825 (circRNA trefoil factor 1, circ_TFF1) in BC pathogenesis.

The expression levels of circ_0061825, miR-593-3p and fibroblast growth factor receptor 3 (FGFR3) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Circ_0061825 was characterized using ribonuclease (RNase) R digestion, actinomycin D and subcellular fractionation assays. Cell viability, colony formation, migration, invasion, cell cycle progression and apoptosis were evaluated using Cell Counting Kit-8 (CCK-8), colony formation, wound-healing, transwell and flow cytometry assays, respectively. Targeted relationships among circ_0061825, miR-593-3p and FGFR3 were determined by a dual-luciferase reporter assay. Animal studies were used to assess the impact of circ_0061825 i circ_0061825, an up-regulated circRNA in BC, regulated BC malignant progression at least in part through targeting the miR-593-3p/FGFR3 axis, illuminating a novel therapeutic target for BC management.
To investigate the genes of patients with sporadic endometrial cancer (EC) and suspected Lynch syndrome (LS)-related EC in the Chinese population. Identification of meaningful mutation sites can provide theoretical basis for molecular targeted therapy, aiming to improve the prognosis of patients with EC.

We recruited 388 patients with EC for mismatch repair (MMR) immunohistochemistry and MLH1 methylation analysis. Based on the results, they were divided into four groups MMR without deletion group (sporadic EC group 1); MLH1&PMS2 deletion and MLH1 methylation group (sporadic EC group 2); MSH2 and/or MSH6 deletion group (suspected LS group); and unclassified group (remainder cases). Patients from each group were randomly screened for whole-exome sequencing detection. Genome Analysis Toolkit, VarScant, MuTect, and CONTRA were used to detect the insertions/deletions, single nucleotide polymorphisms, and copy number variations. Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichmeNPCL1, PRAMEF1, CFAP74, and DFFB may be potential biomarkers for EC or LS-related EC.
The initiation and progression of colorectal cancer (CRC) are a multistep complex process regulated by multiple factors. Previous evidence indicated that microRNA-802 (miR-802) participated in tumorigenesis of numerous solid cancers; however, the potential roles and underlying mechanisms of miR‑802 in CRC still need further exploration.

Quantitative real-time PCR (qRT-PCR) was employed to evaluate miR-802 levels in human CRC tissues and cell lines. In vitro proliferation, apoptosis, migration and invasion assays, and in vivo subcutaneous mouse xenograft model were utilized to examine the effects of miR-802 on the malignant behaviors of CRC cells. Then, bioinformatics prediction, dual-luciferase reporter, qRT-PCR, and Western blot was conducted to confirm the down-stream target of miR-802.

MiR-802 was frequently down-regulated in CRC tissues and cells. Further analyses showed that the low expression of miR-802 in CRC tissues was significantly correlated with tumor progression and poor patients' prognosis.
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