Notes

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The incidence and mortality of lung cancer continue to increase around the world; in 2018, new lung cancer cases accounted for 11.6% of all cancer cases, and lung cancer deaths accounted for 18.4% of cancer deaths. Cisplatin (DDP) is a first-line chemotherapy drug for lung cancer; however, DDP resistance can lead to a poor prognosis in patients with lung cancer. Therefore, reversing DDP resistance is a treatment goal.

Cell counting kit-8 (CCK8) assays, wound healing analyses, Transwell assays, in vitro tumor xenografts, and flow cytometry were used to detect the proliferation, migration, invasion, and apoptosis of multidrug resistant A549/DDP and PC9/DDP cells, respectively. Western blot was performed to detect protein levels of cleaved caspase-3, CHOP, and GRP78.

Delicaflavone inhibited DDP resistance of lung cancer cells and decreased proliferation in a dose- and time-dependent manner. It also decreased migration and invasion and enhanced apoptosis. Western blots showed that delicaflavone overcame DDP resistance by increasing the expression of GRP78 and CHOP and the apoptosis-related protein cleaved caspase-3.

Delicaflavone can reverse DDP resistance in A549/DDP and PC9/DDP cells by inhibiting cell proliferation and migration and enhancing apoptosis and cleaved caspase-3 levels by increasing the expression of CHOP and GRP78 protein via the endoplasmic reticular stress pathway. It could be a useful therapeutic adjunct to treat DDP-resistant lung cancer.
Delicaflavone can reverse DDP resistance in A549/DDP and PC9/DDP cells by inhibiting cell proliferation and migration and enhancing apoptosis and cleaved caspase-3 levels by increasing the expression of CHOP and GRP78 protein via the endoplasmic reticular stress pathway. It could be a useful therapeutic adjunct to treat DDP-resistant lung cancer.
Paclitaxel is widely used in the treatment of cancer and has a good effect in the treatment of non-small cell lung cancer. The combination of TMT proteomics and bioinformatics is used to systematically analyze the molecular mechanism of paclitaxel in the treatment of lung adenocarcinoma A549 cell, which is helpful to screen new therapeutic targets.

MTT assay was used to analyze the inhibitory effect of paclitaxel on the proliferation of A549 cells. The proteins were identified by TMT quantitative proteomics and the differential expression proteins (DEPs) database was constructed. The DEPs were enriched by Gene Ontology (GO) and KEGG pathway annotation. Based on the information in the STRING database, find the interaction between DEPs, and the protein-protein interaction (PPI) networks of DEPs were constructed and analyzed by using the Cytoscape software. According to the PPI network results, select the hub proteins from DEPs for WB verification.

A total of 5449 proteins were identified in A549 by TMT pr pathways, thus killing lung adenocarcinoma cell A549. These findings will enhance the understanding of the mechanism of paclitaxel in the treatment of lung adenocarcinoma cell A549 and provide new valuable targets.
Paclitaxel significantly increased the expression of tubulin, binding tubulin to promote A549 cell death. In addition, paclitaxel significantly inhibited the expression of hub proteins, DNA replication and cell cycle pathways, thus killing lung adenocarcinoma cell A549. These findings will enhance the understanding of the mechanism of paclitaxel in the treatment of lung adenocarcinoma cell A549 and provide new valuable targets.
Lymph node metastasis is one of the important prognostic factors of colorectal cancer, and an important index of individualized treatment. The purpose of this study is to use metabonomics to identify potential molecular markers of lymph node metastasis in colorectal cancer (CRC).

Peripheral blood samples of 223 CRC patients were collected. The metabolic levels of amino acids and carnitine in peripheral blood of CRC patients, with and without lymph node metastasis, were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS).

The results show that there were significant differences in the levels of serum amino acids and carnitine between lymph node metastatic patients and lymph node non-metastatic patients. The diagnostic model that was constructed by 9 types of serum metabolites has a high diagnostic ability.

LC-MS/MS is a detection method that has a broad application in predicting CRC prognosis, individualized treatment, and in studying the mechanism of lymph node metastasis.
LC-MS/MS is a detection method that has a broad application in predicting CRC prognosis, individualized treatment, and in studying the mechanism of lymph node metastasis.
Radiotherapy is one of the most important methods in the treatment of patients with hypopharyngeal squamous cell carcinoma (HSCC). However, radioresistance will be developed after repeated irradiation. Among many key factors contributing to radioresistance, enhanced autophagy is recognized as one of the most important. The ultraviolent irradiation resistance-associated gene (UVRAG) is reported to be a crucial gene involved in the process of autophagy. Here, we test whether UVRAG has effect on the radioresistance of HSCC.

HSCC cell line Fadu cells were treated with irradiation to test levels of autophagy. Tumor tissues from primary and recurrent HSCC patients were tested by immunohistochemistry. Then, we knocked down UVRAG to test its role in cell growth and the malignant behaviors. Response of cells to treatment was examined using LDH release assay, immunofluorescence, Western blot analysis and colony formation.

We found that irradiation induced autophagy in Fadu cells. Immunohistochemistry of primary and irradiated HSCC tumor tissues showed that UVRAG was upregulated after irradiation treatment. Inhibiting UVRAG with siRNA interfered cell growth, cell cycle, malignant behaviors and autophagic flux in Fadu cells. Knocking down UVRAG increased DNA damage and cell death induced by irradiation. Finally, we found that inhibiting UVRAG induced lysosomal membrane permeabilization, which contributed to radiosensitization of Fadu cells.

Our findings supported the oncogenic properties of UVRAG in HSCC and inhibiting UVRAG increased radiosensitivity in HSCC by triggering lysosomal membrane permeabilization. Therefore, UVRAG might be a promising target in the treatment of HSCC.
Our findings supported the oncogenic properties of UVRAG in HSCC and inhibiting UVRAG increased radiosensitivity in HSCC by triggering lysosomal membrane permeabilization. Therefore, UVRAG might be a promising target in the treatment of HSCC.
The majority of patients with hepatocellular carcinoma (HCC) are diagnosed at an advanced stage that excludes them from potentially curative surgical treatment. Lenvatinib is associated with a high objective response rate (ORR) (40.6%) in advanced HCC, indicating the potential for tumor downstaging and conversion to surgical intervention. We report the case of a patient with recurrent, advanced HCC who achieved a partial response and downstaging following third-line treatment with lenvatinib but missed the opportunity for conversion hepatectomy.

A male Chinese patient aged 42 years presented with an obstructive liver lesion, revealed by CT imaging to be a single tumor in segments V and VIII of the liver, without macrovascular invasion. buy Nazartinib The patient had chronic hepatitis B infection, Barcelona Clinic Liver Cancer (BCLC) Stage A, normal liver function (Child-Pugh Score 5 and Grade A) and AFP level 4.45 ng/mL. The patient underwent a successful hepatectomy but experienced recurrence 14 months later. The recury or liver transplantation, should be undertaken quickly following downstaging and within the expected PFS time associated with lenvatinib. However, further studies are required to provide additional evidence for this treatment strategy.
Non-small cell lung cancer (NSCLC) is a heterogeneous tumor that accounts for approximately 85% of all lung cancer cases worldwide. microRNAs (miRNAs) are believed to play an important role in regulating a variety of biological processes, including immunity and cancer. We investigated the effect of miR-519d-3p on the mitigation of NSCLC in vitro and in vivo.

RT-PCR or immunohistochemical assays were used to assess the expression of miR-519d-3p. Colony formation, flow cytometry, and transwell assay were respectively used to detect proliferation, apoptosis, and invasion of A549 and NCI-H661 cell lines. Luciferase reporter assay was used to verify targeting the relationship between mir-519d-3p and VEGFA. Western blot was used to examine the expression of Ki67, caspase-3, E-cadherin, N-cadherin, VEGF, P38, and PI3K/AKT. Animal models were established by BABL/c mice to research the effect of mir-519d-3p overexpression in vivo.

In vitro, miR-519d-3p overexpression inhibited A549 and NCI-H661 cells proliferation, invasion, and also promoted apoptosis. In addition, miR-519d-3p overexpression downregulated VEGFA expression and decreased the P38 and PI3K/AKT phosphorylation level. In vivo, miR-519d-3p overexpression significantly restrained tumor volume (2087±265 mm
vs 599±135 mm
,
< 0.05) and tumor weight (0.45±0.08 g vs 0.13±0.06 g,
<0.05) compared with the control group. Overexpression of miR-519d-3p downregulated levels of Ki67 and N-cadherin significantly.

The data indicated that miR-519d-3p could be a novel therapy or adjuvant against NSCLC.
The data indicated that miR-519d-3p could be a novel therapy or adjuvant against NSCLC.
Cervical cancer is the second most prevalent female malignance, and human papillomavirus (HPV) infection is the main pathogenic factor of cervical cancer. Emerging evidence has revealed that a number of long non-coding RNAs (lncRNAs) play critical roles in the tumorigenesis and progression of cervical cancer. The aim of this study was to further investigate the precise role of lncRNA LINC00511 in HPV-negative and HPV-positive cervical cancer cells and explore the potential regulatory mechanism.

The expression of LINC00511 in cervical cancer and cell lines was examined by RT-PCR. Fluorescence in situ hybridization analysis (FISH) assay was performed to detect the localization of LINC00511 in cervical cancer cells. Loss-of-function experiments of LINC00511 by siRNA interference were performed to assess its effects on HPV-negative and HPV-positive cervical cancer cells. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to identify the target of LINC00511. Relative expression of relad invasion, which could be reversed by miR-324-5p mimics or si-LINC00511.

Collectively, these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.
Collectively, these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.
Glioma is a fatal primary malignant tumor. We aimed to explore the effect of nuclear receptor subfamily 5 group A member 2 (
) on glioma.

expression in glioma tissues and cells was detected using qRT-PCR and immunohistochemistry (IHC)/Western blot. SPSS 22.0 was performed to explore the relationship between
expression and glioma clinicopathologic features. The down-expressed plasmid of
was transfected into glioma cells, and the cell viability, proliferation, apoptosis, migration, and invasion were respectively determined by MTT, EdU, flow cytometry, wound healing and transwell assays. Cell cycle was analyzed using flow cytometry. Temozolomide (TMZ)-resistant glioma cells were established to define the effect of
on drug resistance. The expressions of Notch pathway-related proteins were assessed by Western blot. Glioma nude mice model was constructed to explore the role of
played in vivo.

was highly expressed in glioma tissues and cell lines.
overexpression was related to the poor prognosis of glioma patients.
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