[Protective effect of hydrogen sulfide on intestinal ischemia/reperfusion injury in rats by regulating c-Jun N-terminal kinase/activator protein-1 signaling pathway].

Objective: To investigate whether hydrogen sulfide (HS) protects against intestinal ischemia/reperfusion (I/R) injury in rats by regulating c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) signaling pathway.

Methods: Thirty male Wistar rats were divided into sham operated group (Sham group), I/R group, and HS donor sodium hydrosulfide (NaHS) intervention group (I/R+NaHS group), with 10 rats in each group. The I/R injury model was established by blocking the superior mesenteric artery with a non-traumatic vascular clip, with 60 minutes of ischemia followed by 120 minutes of reperfusion.

Hepatocyte-specific METTL3 ablation by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and postnatal lethality.

Aim: In 2019, to examine the functions of METTL3 in liver and underlying mechanisms, we generated mice with hepatocyte-specific METTL3 homozygous knockout (METTL3Δhep) by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT) or Alb-Cre mice (JAX), respectively. In this study, we explored the potential reasons why hepatocyte-specific METTL3 homozygous disruption by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and then postnatal lethality.

Main Methods: Mice with hepatocyte-specific METTL3 knockout were generated by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT; Strain No.

Hairy gene homolog increases nasopharyngeal carcinoma cell stemness by upregulating .

B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1) is overexpressed in various cancer types. We found that mRNA levels were elevated in nasopharyngeal carcinoma (NPC) cell lines. In immunohistochemical analyses, high Bmi-1 levels were observed in not only 5 of 38 non-cancerous nasopharyngeal squamous epithelial biopsies, but also in 66 of 98 NPC specimens (67.

Retraction Notice to: LINC00472 Acts as a Tumor Suppressor in NSCLC through KLLN-Mediated p53-Signaling Pathway via MicroRNA-149-3p and MicroRNA-4270.

[This retracts the article DOI: 10.1016/j.omtn.

Activation of the Hedgehog pathway mediates resistance to epidermal growth factor receptor inhibitors in non-small cell lung cancer.

The current study aimed to investigate the function of the Hedgehog pathway and its association with epithelial-mesenchymal transition (EMT) in epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) resistance in non-small cell lung cancer (NSCLC). Lung tumor tissue specimens from EGFR TKI-resistant patients, including those with brain metastases, had hyperactive Hedgehog signaling compared with those from TKI-sensitive patients. SHH stimulation promoted GLI1 activation as well as cell motility in parental PC9 cells while suppressing gefitinib-induced apoptosis in gefitinib-resistant cells.

[Role of hydrogen sulfide on expression of phosphatidylinositol 3 kinase/protein kinase B signal pathway in rats with intestinal ischemia/reperfusion injury].

Objective: To explore the effect of hydrogen sulfide (HS) on expression of phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signal pathway in rats with intestinal ischemia/reperfusion (IRI) injury.

Methods: Thirty male Wistar rats were divided into sham operation group (Sham group), IRI group, and HS precursor sodium hydrosuphide (NaHS) intervention group (IRI+NaHS group) by random number table method, with 10 rats in each group. The animal model of IRI was established by 60 minutes superior mesenteric artery (SMA) blockage with non-invasive vascular clamp and 120 minutes reflow.

A comparative study on etoposide combined with lobaplatin or cisplatin in the first-line treatment of extensive-stage small cell lung cancer.

Purpose: To compare the efficacy and safety of etoposide combined with lobaplatin or cisplatin in the first-line treatment of extensive-stage small cell lung cancer (SCLC).

Methods: A total of 98 extensive-stage SCLC patients treated at the Oncology Department from March 2015 to March 2017 were enrolled and divided into etoposide + lobaplatin group (EL group, n=49) and etoposide + cisplatin group (EP group, n=49) using a random number table. The clinical data of all patients were collected, and the short-term effective rate, changes in the levels of serum tumor markers carcinoembryonic antigen (CEA), cytokeratin 19 fragment (CYFRA21-1) and neurone specific enolase (NSE) before and after chemotherapy and adverse reactions were compared between the two groups.

SHCBP1 promotes cisplatin induced apoptosis resistance, migration and invasion through activating Wnt pathway.

Lung cancer is the leading cause for cancer death due to refractory nature to current treatment strategies, understanding the regulatory mechanism of therapy resistance of lung cancer is important for lung cancer therapy. Here, we aimed to study the role of SHCBP1 in lung cancer cisplatin resistance, we found SHCBP1 was upregulated in lung cancer tissues and cells, patients with high SHCBP1 had poor prognosis. SHC binding and spindle associated 1 (SHCBP1) overexpression promoted cisplatin induced apoptosis resistance, migration and invasion determined by apoptosis assay and transwell assay with or without Matrigel, while SHCBP1 knockdown inhibited cisplatin induced apoptosis resistance, migration and invasion.

LINC00472 Acts as a Tumor Suppressor in NSCLC through KLLN-Mediated p53-Signaling Pathway via MicroRNA-149-3p and MicroRNA-4270.

Long non-coding RNAs and microRNAs (miRNAs) have been reported to participate in the progression of non-small-cell lung cancer (NSCLC). Long intergenic non-protein-coding RNA 472 (LINC00472), miR-149-3p, and miR-4270 were found to be involved in tumor activities, suggesting potential roles in NSCLC. Thus, this study aimed to examine the ability of LINC00472 to influence the progression of NSCLC with the involvement of miR-149-3p and miR-4270.

NEAT1 is a potential prognostic biomarker for patients with nasopharyngeal carcinoma.

Nuclear paraspeckle assembly transcript 1 (NEAT1) has been found to be dysregulated and associated with clinical progression in various human cancers. The clinical and prognostic value of NEAT1 in nasopharyngeal carcinoma (NPC) was still controversial. The aim of our study was to provide more sufficient evidence that NEAT1 expression is correlated with overall survival in patients with NPC.

Concurrent versus sequential whole brain radiotherapy and TKI in EGFR-mutated NSCLC patients with brain metastasis: A single institution retrospective analysis.

To examine the outcomes of concurrent versus sequential whole-brain radiotherapy (WBRT) and epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) in nonsmall cell lung cancer (NSCLC) patients with EGFR mutation.Retrospectively 105 patients with NSCLC, brain metastasis, and EGFR mutation (Affiliated Hospital of Guangdong Medical University, 01/2011 to 12/2014) were grouped as: EGFR-TKIs alone (n = 39, group A), EGFR-TKIs + concurrent radiotherapy (n = 34, group B), and radiotherapy followed by EGFR-TKIs (n = 32, group C).The intracranial objective response rates of groups A, B, and C were 66.

[CK2α Regulates the Metastases and Migration of Lung Adenocarcinoma A549 Cell Line through PI3K/Akt/GSK-3β Signal Pathway].

Background: Lung cancer is the leading cancer-related death worldwide. Patients with lung cancer mainly died of tumor metastasis and invasion. Protein kinase CK2 is an ubiquitous serine/threonine protein kinase and is frequently upregulated in various human tumors.

[Correlation of CD4CD29 regulatory T cells with recurrence and survival time in patients with non-small cell lung cancer].

Objective: To investigate the correlation of CD4CD29 regulatory T cells (Treg) with tumor recurrence and survival time in patients with non-small cell lung cancer (NSCLC).

Methods: Fifty-nine patients with NSCLC treated with radical surgery were followed up for 5 years. Blood Treg cells were examined during the follow-up using flow cytometry (FCM).

LATS2 as a poor prognostic marker regulates non-small cell lung cancer invasion by modulating MMPs expression.

Large tumor suppressor 2 (LATS2) plays significant roles in tumorigenesis and cancer progression. This study was aimed to analyze the correlation between LATS2 expression and clinicopathologic features and its prognostic significance in non-small cell lung cancer (NSCLC). LATS2 expression was examined in 73 NSCLC clinical specimens and 22 normal lung tissues using immunohistochemistry.

[Change in endogeous hydrogen sulfide in patients with acute pancreatitis and its relationship to coagulation function].

Objective: To study the change in endogenous hydrogen sulfide (H2S) in patients with acute pancreatitis and its relationship to coagulation function.

Methods: A prospective case control study was conducted. Forty patients with mild acute pancreatitis (MAP group) and 40 with severe acute pancreatitis (SAP group) admitted to Yiwu Central Hospital in Zhejiang Province from December 2002 to March 2015 were enrolled.

Reduced PDCD4 Expression Promotes Cell Growth Through PI3K/Akt Signaling in Non-Small Cell Lung Cancer.

It is largely recognized that PDCD4 is frequently lost in tumors of various origins, including lung cancer, and its loss contributes to tumor progression. However, its role and molecular mechanism remain largely unexplored in non-small cell lung cancer (NSCLC). In this study, downregulated PDCD4 mRNA expression was found in NSCLC tissues compared to their corresponding paracarcinoma tissues and distal paracarcinoma tissues.

Controversies regarding T status and N status for non-small cell lung cancer.

According to the newest version of NCCN Clinical Practice Guidelines for Non-Small Cell Lung Cancer (NSCLC), increasing attentions are paid to the role of nodal status and other high-risk factors, including vascular invasion, wedge resection, tumors > 4 cm, visceral pleural involvement, and incomplete lymph node sampling in the individual clinical treatment. Precise definitions of T status and N status, closely associated with prognosis and treatment, are worth expanding further. However, complexity arises because no unity definition exists regarding individual T and N descriptors.

High-mobility group A2 overexpression is an unfavorable prognostic biomarker for nasopharyngeal carcinoma patients.

Our previous study showed that knockdown of high-mobility group A2 (HMGA2) could suppress nasopharyngeal carcinoma (NPC) cell migration, invasion, and epithelial-mesenchymal transition (EMT) process, and HMGA2 is a direct functional target of let-7 to regulate NPC cell migration, invasion, and EMT process. However, little is known about the clinical and prognostic significance of HMGA2 protein in NPC patients. The purpose of this study is to identify the clinical and prognostic roles of HMGA2 in NPC patients.

[MiR-373-3p Promotes Invasion and Metastasis of Lung Adenocarcinoma Cells].

Background And Objective: Lung cancer is the leading cause of cancer-related deaths worldwide, and metastasis is the major cause of death in lung cancer patients. MiR-373 is closely associated with invasion and metastasis in other tumor cells. This study explored the expression of miR-373-3p in non-small cell lung cancer (NSCLC) and its effect on the invasive and metastatic capabilities of lung adenocarcinoma cells, as well as their mechanisms of action.

Let-7a inhibits migration, invasion and epithelial-mesenchymal transition by targeting HMGA2 in nasopharyngeal carcinoma.

Background: Let-7a has been shown to play important roles in nasopharyngeal carcinoma (NPC) cell proliferation and apoptosis, but little is known about the function and mechanism of let-7a in nasopharyngeal carcinoma metastasis. We aimed to investigate the function and mechanism of let-7a in nasopharyngeal carcinoma metastasis and clarified the regulation of high mobility group A2 (HMGA2) by let-7a.

Methods: The expression levels of let-7a and HMGA2 were examined in NPC clinical specimens using quantitative reverse transcription-PCR (RT-qPCR).

Upregulation of microRNA-492 induced by epigenetic drug treatment inhibits the malignant phenotype of clear cell renal cell carcinoma in vitro.

Clear cell renal cell carcinoma (ccRCC) is the most common type of cancer of the renal parenchyma. MicroRNAs (miRNAs) are non-coding RNAs of ~22 nucleotides in length, which function as post‑transcriptional regulators. Recently, the downregulation of miRNA (miR)-492 was observed to be associated with ccRCC; however, the molecular mechanism by which miR492 inhibited ccRCC remained to be elucidated.

MMP-14 overexpression correlates with poor prognosis in non-small cell lung cancer.

Matrix metalloproteinase-14 (MMP-14) has been demonstrated to play an important role in tumor progression. The aim of this study was to analyze the correlation between MMP-14 expression and clinicopathologic features and its prognostic significance in non-small cell lung cancer (NSCLC). Immunohistochemical staining for MMP-14 protein was performed in 104 patients with NSCLC.

Knocking down CDK4 mediates the elevation of let-7c suppressing cell growth in nasopharyngeal carcinoma.

Background: CDK4 is a protein kinase in the CDK family important for G1/S phase cell cycle progression. However, the roles and molecular mechanisms of CDK4 triggering nasopharynx carcinogenesis are still unclear.

Methods: Lentiviral-vector mediated shRNA was used to suppress CDK4 expression and examine its molecular mechanisms.

Meta-analysis on the association between pathologic complete response and triple-negative breast cancer after neoadjuvant chemotherapy.

Background: Triple-negative breast cancer (TNBC) is a special subtype of breast cancer that is characterized by poor prognosis, strong tumor invasion and a high pathologic complete response (pCR) to neoadjuvant chemotherapy (NAC). The pCR rate is a prognostic factor for TNBC. We aimed to evaluate the relationship between pCR and TNBC after NAC and originally tried to identify factors related to achieving pCR for TNBC using a meta-analysis.