Hubbardbentzen2035
The results suggest that alum, CpG ODN, and HH2 complex as a novel immune adjuvant combined cancer vaccine could improve the immunity efficiency in a murine multiple myeloma model.
The failure of chemotherapy in osteosarcoma results in drug resistance and acute side effects in the body.
In this study, we have prepared a novel folate receptor-targeted doxorubicin (DOX) and edelfosine (EDL)-loaded lipid-polymer hybrid nanoparticle (DE-FPLN) to enhance the anticancer efficacy in osteosarcoma. The nanoparticles were thoroughly characterized for in vitro biological assays followed by detailed antitumor efficacy analysis and toxicity analysis in a xenograft model.
The dual drug-loaded nanoparticles showed a nanosized morphology and physiological stability. The targeted nanoparticles showed enhanced cellular internalization and subcellular distribution in MG63 cancer cells compared to that of non-targeted nanoparticles. Among many ratios of DOX and EDL, 11 ratiometric combinations of drugs were observed to be highly synergistic in killing the cancer cells. MTT assay and caspase-3/7 activity assay clearly showed the superior anticancer efficacy of DE-FPLN formulations in inducing the cancer cell death. In vitro results indicate that the co-administration of two drugs in a folic acid-targeted nanoparticle could potentially induce the apoptosis and cell death. In vivo results displayed the potency of tumor cell killing and significant suppression of tumor growth without any detectable side effects.
The lipid-polymer hybrid nanocarriers with multiple properties of high drug loading, sequential and ratiometric drug release, improved physiological stability, prolonged blood circulation, and tumor-specific targeting are promising for the delivery of multiple drugs in the treatment of osteosarcoma.
The lipid-polymer hybrid nanocarriers with multiple properties of high drug loading, sequential and ratiometric drug release, improved physiological stability, prolonged blood circulation, and tumor-specific targeting are promising for the delivery of multiple drugs in the treatment of osteosarcoma.Immune cells are essential for defending the body's balance and have increasingly been implicated in controlling tumor growth. In cervical cancer (CC), the immune landscape is extensively connected with human papillomavirus (HPV) status. Recent insights from studies have revealed that as a result of infection with HPV, immune cell populations such as lymphocytes or monocytes change during carcinogenesis. Immune therapy, in particular checkpoint inhibitors, those targeting PD-1 or PD-L1, has shown promising efficacy. This article reviews the immune landscape and immunotherapy of CC.
MiR-654-3p plays important roles in many types of malignant tumours. However, the biological function of miR-654-3p in non-small cell lung cancer (NSCLC) remains unknown. In this study, the role of miR-654-3p in NSCLC was investigated.
qRT-PCR was used to evaluate the level of miR-654-3p in NSCLC tissues and cell lines, while Cell Counting Kit-8, Annexin V/propidium iodide dual staining or TUNEL staining were used to investigate proliferation and apoptosis of NSCLC cells. Luciferase assays and Western blotting were performed to validate potential targets of miR-654-3p.
MiR-654-3p levels were significantly decreased in NSCLC patients and cell lines and were significantly correlated with the tumour size and tumour node metastasis stage of NSCLC patients. In A549 cells, miR-654-3p overexpression significantly increased apoptosis and inhibited growth both in vivo and in vitro, while downregulation of miR-654-3p had the opposite effects. In addition, polo-like kinase 4 (PLK4) was shown to be a target gene of miR-654-3p that is negatively regulated by miR-654-3p in A549 cells. Furthermore, PLK4 was observed to be highly expressed in NSCLC tissues and cells, and PLK4 overexpression abolished the inhibitory effects of miR-654-3p overexpression on NSCLC cell proliferation. Finally, the animal experiment results further demonstrated that miR-654-3p inhibits tumour growth and regulates PLK4 expression.
Our results demonstrate that miR-654-3p functions as a growth-suppressing miRNA by targeting PLK4 in NSCLC.
Our results demonstrate that miR-654-3p functions as a growth-suppressing miRNA by targeting PLK4 in NSCLC.
The study aimed to explore the mechanism of miR-133b regulating the invasion and migration of gastric cancer (GC) cells via the COL1A1/TGF-β axis.
The miRNA expression profiles of GC downloaded from TCGA database were subjected to differential analysis to determine the target miRNA of interest, and the target genes of the miRNA were predicted by bioinformatics. GSEA was used for gene enrichment analysis. qRT-PCR was carried out to detect gene expression in GC cells. The effect of miR-133b on GC cells was examined by CCK-8, wound healing and Transwell assays. Western blot was conducted to assess the protein expression of EMT-related proteins. The binding relationship between genes was verified by dual-luciferase reporter gene assay.
The expression of miR-133b was markedly downregulated in GC tissue, while that of COL1A1 was upregulated. Overexpression of miR-133b decreased the migration and invasion of GC cells, and the EMT process was inhibited as well, while inverse results were observed when miR-133b was silenced. COL1A1 was a target gene of miR-133b and its overexpression had a significant impact on the prognosis of patients. GSEA pathway enrichment results showed that COL1A1 was markedly enriched in the TGF-β signaling pathway. In addition, COL1A1 overexpression induced the activation of the TGF-β signaling pathway to promote proliferation and migration of GC cells, whereas miR-133b overexpression suppressed the signaling pathway. Thus, overexpression of miR-133b and COL1A1 simultaneously would reverse the inhibitory effect of miR-133b on cell invasion and migration.
In this study, miR-133b was found to inhibit the invasion and migration of GC cells via the COL1A1/TGF-β axis, which provides a new research direction for the diagnosis and targeted therapy of GC.
In this study, miR-133b was found to inhibit the invasion and migration of GC cells via the COL1A1/TGF-β axis, which provides a new research direction for the diagnosis and targeted therapy of GC.
Long non-coding RNAs (lncRNAs) have been reported to play important roles in tumor biology. In this study, we aimed to investigate the effects of T-box transcription factor 5 antisense RNA 1 (
) on aggressive phenotypes of non-small cell lung cancer (NSCLC) cells and explore its regulatory pathway.
The expression of
in tissues, plasma, and cells was determined by qRT-PCR. Cell viability, proliferation, migration, invasion, and apoptosis were assessed using MTT, colony formation, wound-healing, Transwell, and flow cytometry assay, respectively. Western blot analysis was performed to measure the expression of apoptosis-related proteins. Besides, transfected cells were exposed to PI3K activator (740Y-P) to verify the regulatory pathway.
TBX5-AS1 expression was down-regulated in NSCLC tissues, plasma, and cells, and associated with lymph node metastasis and histological grade. Overexpression of
inhibited cell viability, colony formation, migration, and invasion, while it promoted apoptosis. Converselugh inactivating the PI3K/AKT pathway. This finding provided a novel insight into NSCLC pathogenesis.
Prostate cancer (PCa) is one of the most common cancers in men worldwide. Early detection of prostate cancer by prostate-specific antigen (PSA) screening still has limitations. The discovery of new candidates is urgent and can provide insights into the mechanism involved in prostate cancer tumorigenesis.
We conducted a cross-sectional study involving prostate cancer cell lines and clinical samples. qPCR and IHC were used to evaluate the expression of miR-137-3p/JNK3/EZH2. Furthermore, cell growth, migration, invasion, cell cycle and apoptosis were analyzed to describe the function of this axis. Moreover, xenograft models, pathology platforms and TCGA data were generated to confirm the role of the miR-137-3p/JNK3/EZH2 axis.
In this study, we determined that miR-137-3p was significantly reduced in prostate cancer, and low expression of miR-137-3p was correlated with tumor stage . The overexpression of miR-137-3p suppressed cell proliferation, migration and invasion in prostate cancer by enhancing cell apoptosis. We also validated JNK3 (MAPK10) as a direct target gene of miR-137-3p. Down-regulation of JNK3 in prostate cancer also inhibited cell proliferation and invasion and promoted apoptosis. Moreover, JNK3 expression was up-regulated and negatively correlated with miR-137-3p in prostate cancer tissues. AUNP12 Furthermore, JNK3 modulated EZH2 expression, which is a key oncogene in prostate cancer. Survival data indicated that patients with high levels of JNK3 and EZH2 had a worse prognosis.
Collectively, the identification of miR-137-3p and the JNK3/EZH2 pathway might facilitate the development of biomarkers and therapeutic targets for prostate cancer.
Collectively, the identification of miR-137-3p and the JNK3/EZH2 pathway might facilitate the development of biomarkers and therapeutic targets for prostate cancer.
The novel Hsp90 inhibitor SNX-2112 showed broad antitumor activity. However, it was still necessary to optimize the therapeutic dosage of SNX-2112 applied on tumors to obtain effective therapy with minimal dose to reduce toxicity. We investigated the role of low-intensity US in promoting antitumorigenic effect of low doses of SNX-2112 on tongue squamous cell carcinoma.
Cell viability was measured using CCK-8 assay or staining with Calcein AM/PI. Relative cumulative levels of SNX-2112 in cells were detected using high-performance liquid chromatography. The production of ROS was analyzed using fluorescence microscope and flow cytometer. Cellular apoptosis was detected using flow cytometer. The expression levels of proteins of the ERS-associated apoptosis signaling pathway were detected using Western blotting analysis. The efficacy and biosafety of SNX-2112 were also investigated in a mouse xenograft model.
Low-intensity US combined with SNX-2112 exhibited significant antitumor effect, increased the absorp reduce the dosage of SNX-2112 required and its side effects.
The antitumor effects of SNX-2112 were enhanced by low-intensity US. The most probable mechanism was that US sonoporation induced more SNX-2112 delivery to the cells and enhanced ROS production, triggering the ERS-associated apoptosis signaling pathway. Therefore, low-intensity US may increase the efficiency of conventional chemotherapy and reduce the dosage of SNX-2112 required and its side effects.
Long non-coding RNAs (lncRNAs) are involved in the development of various tumors including prostate cancer. The purpose of this study was to explore the function of a natural antisense RNA,
, exerting potential carcinogenic effects in prostate cancer through a novel molecular mechanism.
GEPIA and CCLE databases were searched to identify alterations in the expression of
, which were then verified by RT-qPCR in 20 pairs of matched tumor and normal tissue samples. Subsequently, CCK-8, EdU, and transwell assays were conducted to investigate the carcinogenic effect of
. RT-qPCR, Western blot, and isocitrate dehydrogenase 1 (IDH1) enzyme activity assays were used to explore the functional relationship between
and its sense gene IDH1.
IDH1-AS1 expression was found to be significantly increased in prostate cancer tissues and cell lines.
knockdown significantly inhibited the proliferation and migration of prostate cancer cells. Interestingly, RT-qPCR and Western blot analyses revealed that
did not significantly affect the expression of IDH1 mRNA or protein but was involved in the regulation of IDH1 enzyme activity in prostate cancer cells.
