RAMP2-AS1 stabilized RAPM2 mRNA through TIA1 to inhibit the progression of non-small cell lung cancer.

As the most common subtype of lung cancer, non-small cell lung cancer (NSCLC)is responsible for a large proportion of global cancer-caused deaths. The implication of long non-coding RNAs (lncRNAs) as tumor-suppressor or carcinogenic genes in NSCLC has been widely documented. Our study sought to investigate the performance of lncRNA RAMP2 antisense RNA1 (RAMP2-AS1) in NSCLC.

Circ_ATAD3B inhibits cell proliferation of breast cancer via mediating the miR-570-3p/MX2 axis.

It has been discovered that some circular RNAs can serve as excellent therapeutic targets for breast cancer (BC). However, the biological role that circ ATAD3B plays in BC is not yet completely understood. As a result, the purpose of this work was to evaluate the function of circ_ATAD3B in the development of BC.

[Clinical Analysis of Patient with Esophageal Granulocytic Sarcoma Derived from Chronic Myelocytic Leukemia].

Objective: To investigate the diagnosis and treatment of esophageal granulocytic sarcoma derived from chronic myelocytic leukemia (CML).

Methods: The clinical manifestations, diagnosis and treatment of 1 case of esophageal granulocytic sarcoma secondary from chronic myelocytic leukemia were retrospectively analyzed and the related literature was reviewed.

Results: The patient was a 72-year-old woman with poststernal pain accompanied by general weakness.

LncRNA RUSC1-AS1 promotes the proliferation of hepatocellular carcinoma cells through modulating NOTCH signaling.

The long non-coding RNA (lncRNA) RUSC1-AS1 has been reported to be dysregulated in the progression of many cancers. Also, RUSC1-AS1 had been detected to be highly expressed in laryngeal squamous cell carcinoma and breast cancer cells, suggesting that RUSC1-AS1 may be a biomarker for cancers. However, the biological role and regulatory mechanism of RUSC1-AS1 in hepatocellular carcinoma (HCC) remain unknown.

Decreased miR-124 contributes to the epithelial-mesenchymal transition phenotype formation of lung adenocarcinoma cells via targeting enhancer of zeste homolog 2.

Introduction: MiR-124, a tumor suppressor, is involved in regulating various cellular processes. The purpose of this study was to investigate the possible function of miR-124 in LA (lung adenocarcinoma) cells.

Aims: MiR-124 expression levels in the 54 pairs of LA tissues (and corresponding non-tumor tissues) obtained at the Sixth People's Hospital of Yancheng City and in LA cells were assessed by qRT-PCR.

Aurora-A/NF-ĸB Signaling Is Associated With Radio-resistance in Human Lung Adenocarcinoma.

Background/aim: This study aimed to discuss the effect and possible molecular mechanisms of Aurora-A/NF-ĸB signaling on the radiotherapy resistance of human docetaxel-resistant lung adenocarcinoma cells.

Materials And Methods: The human lung adenocarcinoma SPC-A1 and SPC-A1/DTX cell lines were utilized in the present study. The MTT assay measured the sensitivity of cells to radiotherapy.

SQLE induces epithelial-to-mesenchymal transition by regulating of miR-133b in esophageal squamous cell carcinoma.

Increasing evidence suggests that microRNAs, which control gene expression at the post-transcriptional level, are aberrantly expressed in cancers and play significant roles in carcinogenesis and cancer progression. In this study, we show differential miR-133b down-expression in human esophageal squamous cell carcinoma (ESCC) cells and tissues. In addition, squalene epoxidase (SQLE), a key enzyme of cholesterol synthesis, is identified as the direct downstream target gene of miR-133b by luciferase gene reporter assay.

Decreased TUSC3 Promotes Pancreatic Cancer Proliferation, Invasion and Metastasis.

Pancreatic cancer is an aggressive disease with dismal prognosis. It is of paramount importance to understand the underlying etiological mechanisms and identify novel, consistent, and easy-to-apply prognostic factors for precision therapy. TUSC3 (tumor suppressor candidate 3) was identified as a potential tumor suppressor gene and previous study showed TUSC3 is decreased in pancreatic cancer at mRNA level, but its putative tumor suppressor function remains to be verified.

Metabolomics analysis reveals the association between lipid abnormalities and oxidative stress, inflammation, fibrosis, and Nrf2 dysfunction in aristolochic acid-induced nephropathy.

Alternative medicines are commonly used for the disease prevention and treatment worldwide. Aristolochic acid (AAI) nephropathy (AAN) is a common and rapidly progressive interstitial nephropathy caused by ingestion of Aristolochia herbal medications. Available data on pathophysiology and molecular mechanisms of AAN are limited and were explored here.

Enhanced renoprotective effect of HIF-1α modified human adipose-derived stem cells on cisplatin-induced acute kidney injury in vivo.

Current therapeutic options for acute kidney injury (AKI) are limited to the use of supportive measures and dialysis. A recent approach that has sparked great interest and gained enormous popularity is the implantation of stem cells to repair acutely damaged kidney organ. Hypoxia inducible factor-1α (HIF-1α) is effective in protecting the kidney from ischemia and nephrotoxicity.

Human adipose-derived stem cells modified by HIF-1α accelerate the recovery of cisplatin-induced acute renal injury in vitro.

Human adipose-derived stem cells (hASCs) improve renal function in acute kidney injury. Hypoxia-inducible factor-1α (HIF-1α) was transfected into hASCs. hASCs modified by lentivirus-mediated empty-vector and HIF-1α maintained their stem cell characteristics.

Reprogramming of mouse renal tubular epithelial cells to induced pluripotent stem cells.

Kidney disease has reached epidemic proportions and is associated with high mortality and morbidity rates. Stem cell-based therapy may effectively treat kidney damage by cell transplantation. The breakthrough discovery using a combination of four transcription factors to reprogram genetically somatic cells into induced pluripotent stem (iPS) cells was a milestone in stem cell therapy.

Atrogin-1 affects muscle protein synthesis and degradation when energy metabolism is impaired by the antidiabetes drug berberine.

Objective: Defects in insulin/IGF-1 signaling stimulate muscle protein loss by suppressing protein synthesis and increasing protein degradation. Since an herbal compound, berberine, lowers blood levels of glucose and lipids, we proposed that it would improve insulin/IGF-1 signaling, blocking muscle protein losses.

Research Design And Methods: We evaluated whether berberine ameliorates muscle atrophy in db/db mice, a model of type 2 diabetes, by measuring protein synthesis and degradation in muscles of normal and db/db mice treated with or without berberine.

Protective effect of erythropoietin against aristolochic acid-induced apoptosis in renal tubular epithelial cells.

The goal of this research was to investigate the renoprotective effect of erythropoietin against aristolochic acid-induced apoptosis in cultured LLC-PK1 cells as well as underlying mechanism. LLC-PK1 cells impaired by aristolochic acid were used in this study as the cell model of aristolochic acid nephropathy. Apoptosis was studied by different methods (transmission electron microscopy, fluorescence-activated cell sorting, TUNEL, caspase-3 activation).