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Oral squamous cell carcinoma is one of the most common causes of malignancy-associated death. Early diagnosis of oral squamous cell carcinoma (OSCC) is important in patient treatment and prognostic evaluation. Due to the lack of significant therapeutic benefit, the 5-year survival rate has not improved. Therefore, effective novel markers are needed to improve diagnosis. To determine novel promising diagnostic biomarkers for OSCC, 416 upregulated and 416 downregulated differentially expressed genes were screened from OSCC tissues using an RNA microarray. The results suggested that minichromosome maintenance protein (MCM5) mRNA was significantly overexpressed in OSCC tissues compared with that in adjacent normal tissues. Moreover, silencing of MCM5 expression an OSCC cell line (SCC-15) significantly impaired proliferation and colony formation. Furthermore, negative regulation of the mRNA and protein expression of MCM5 and demonstrated that MCM5 served as a cancer-promoting gene modulating OSCC cell proliferation through induced G2/M phase arrest. In this process, the mRNA expression of cyclin E and cyclin-dependent kinase 2 was downregulated, while p21 expression was upregulated. These results suggested that MCM5 may be an important pathogenic factor of OSCC. High expression levels of MCM5 may serve as a marker for the early diagnosis of OSCC.Current chemotherapeutic agents against esophageal cancer (EC) are suboptimal. To improve treatment efficacy, a nanoplatform based on ATP-responsive drug release was developed for EC therapy. First, the chemotherapeutic agent epirubicin (EPI) was inserted into an ATP aptamer (Ap) to form double-stranded DNA ('DNA duplex'). Subsequently, polyethyleneimine (PEI) was employed to condense the EPI-loaded duplex to construct the final nanoplatform (PEI-Ap-EPI). Following internalization by cancer cells, the EPI-loaded DNA duplex could open and release EPI in an intracellular ATP-rich environment. An in vitro drug-release assay demonstrated that ~50% of EPI was released from PEI-Ap-EPI in an ATP-rich condition. However, only 15% of EPI was released in the presence of a low concentration of ATP. In vitro cytotoxicity and apoptosis assays demonstrated that PEI-Ap-EPI could enhance EPI efficiency against EC cells markedly compared with those in the control group. Therefore, this facile PEI-Ap-EPI nanoplatform may be a promising strategy to improve the efficacy of EPI treatment in EC.Cbp/P300 interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) is a transcription co-factor that interacts with several other transcription factors and co-factors, and serves critical roles in fundamental cell processes, including proliferation, apoptosis, differentiation, migration and autophagy. The interacting transcription factors or co-factors of CITED2 include LIM homeobox 2, transcription factor AP-2, SMAD2/3, peroxisome proliferator-activated receptor γ, oestrogen receptor, MYC, Nucleolin and p300/CBP, which regulate downstream gene expression, and serve important roles in the aforementioned fundamental cell processes. Emerging evidence has demonstrated that CITED2 serves an essential role in embryonic and adult tissue stem cells, including hematopoietic stem cells and tendon-derived stem/progenitor cells. Additionally, CITED2 has been reported to function in different types of cancer. Although the functions of CITED2 in different tissues vary depending on the interaction partner, altered CITED2 expression or altered interactions with transcription factors or co-factors result in alterations of fundamental cell processes, and may affect stem cell maintenance or cancer cell survival. The aim of this review is to summarize the molecular mechanisms of CITED2 function and how it serves a role in stem cells and different types of cancer based on the currently available literature.Parvimonas micra (P. micra) is reported to be associated with colorectal cancer (CRC). However, its association with colorectal adenoma (CRA) and its role in the initiation of colorectal tumors remain unknown. The present study aimed to clarify the relationship between P. micra and CRA and CRC by exploring the changes of P. find more micra abundance in an adenoma-carcinoma sequence in a new cohort and 4 public sequencing datasets. To investigate the alterations of P. micra abundance in the gut along the adenoma-carcinoma sequence, quantitative PCR (qPCR) was conducted to measure the relative abundance of P. micra in fecal samples from 277 subjects (128 patients with CRA, 66 patients with CRC and 83 healthy individuals, as controls) who underwent colonoscopy as outpatients. Then, the relative abundance of P. micra was analyzed in fecal samples from 596 subjects (185 healthy controls, 158 CRC, 253 CRA) in four public 16S rRNA sequencing datasets. The qPCR results demonstrated that the CRA group had an abundance of P. micra (P=0.2) similar to that of the healthy control group, while the CRC group had a significantly increased abundance (P=8.2×10-11). The level of P. micra effectively discriminated patients with CRC from healthy controls, while it poorly discriminated patients with CRA from healthy controls; with an area under the receiver operating characteristic curve of 0.867 for patients with CRC and 0.554 for patients with CRA. The same pattern of the alteration of P. micra abundance, which was low in healthy controls and patients with CRA but elevated in patients with CRC, was found in all four public sequencing datasets. These results suggested that P. micra was closely associated with, and may serve as a diagnostic marker for, CRC but not CRA. Moreover, it was indicated that P. micra may be an opportunistic pathogen of CRC, which may promote CRC development but serve a limited role in tumorigenesis.Long non-coding RNAs (lncRNAs) serve important regulatory roles in human tumors. The aim of the present study was to examine the role of ribonuclease P RNA component H1 (RPPH1) in non-small cell lung cancer (NSCLC). RPPH1 expression was assessed in datasets from The Cancer Genome Atlas, as well as lung cancer cell lines and patients with NSCLC. RPPH1 was significantly upregulated in NSCLC cell lines, compared with a normal lung epithelial cell line. Moreover, high RPPH1 expression was associated with poor overall survival and disease progression. RPPH1 was knocked down in A549 and H1299 cells using short hairpin (sh) RNA constructs, and the expressions of target genes and proteins were determined by reverse transcription-quantitative PCR and western blotting. Cell invasion potential was also determined using Transwell Matrigel assays. Compared with the negative control, RPPH1 silencing significantly reduced the number of invading cells, increased E-cadherin expression and reduced vimentin protein expression. Cell resistance to cisplatin/cis-diamminedichloridoplatinum (CDDP) was also evaluated using Cell Counting Kit-8 and colony formation assays.