LncRNAs are involved in many physiological and pathological processes, including chromatin remodeling, transcription, posttranscriptional gene expression, mRNA stability, translation, and posttranslational modification, and their functions depend on subcellular localization. MIR503HG is a lncRNA as well as a host gene for the miRNAs miR-503 and miR-424. MIR503HG functions independently or synergistically with miR-503. MIR503HG affects cell proliferation, invasion, metastasis, apoptosis, angiogenesis, and other biological behaviors. The mechanism of MIR503HG in disease includes interaction with protein, sponging miRNA to regulate downstream target gene, and participation in NF-κB, TGF-β, ERK/MAPK, and PI3K/AKT signaling pathways. In this review, we summarize the molecular mechanisms of MIR503HG in disease and its potential applications in diagnosis, prognosis, and treatment. We also raise some unanswered questions in this area, providing insights for future research.

HPV genotypes were determined in 63 vaginal intraepithelial neoplasia (VaIN) and 7 vaginal squamous cell carcinomas (VaSCC). Of these, 37 cases had VaIN alone, and 26 cases had both VaIN and cervical intraepithelial neoplasia (CIN) or condyloma. HPV typing was performed in scraped cells by Genosearch-31 (GS-31) and in the archived tissues by uniplex E6/E7 PCR. In a total of 49 VaIN1, 17 VaIN2/3, and 7 VaSCC tissues, the prevalence of HPV was 91.2% in VaIN (VaIN1: 87.8%, VaIN2/3: 100%) and 85.7% in VaSCC. Comparing HPV results in scraped cell and tissue, 46.2% of high-risk (HR) types and 68.1% of any HPV types that had been identified in cell samples were not present in corresponding tissues. HPV types in VaIN and CIN lesions differed in 92.3% (24/26) of cases with multiple lesions. These results suggest that there are many preclinical HPV infections in the vagina or the cervix, and VaIN and CIN are independently developed. The manual microdissection procedure of tissue revealed one HPV type in one lesion. Seventeen HPV types, including high-risk (HR), possible high-risk (pHR), and low-risk (LR), were identified in 43 VaIN1 lesions. In higher grade lesions, six HR (HPV16, 18, 51, 52, 56, 58), one pHR (HPV66), and one LR (HPV42) HPV types were identified in 17 VaIN2/3, and six HPV types, including HPV16, 45, 58, and 68 (HR), and HPV53 and 67 (pHR), were detected in each case of VaSCC. The vagina appears to be the reservoir for any mucosal HPV type, and HR- or pHR-HPV types are causative agents for vaginal malignancies.

Long non-coding RNAs (lncRNAs) are non-protein coding RNAs with more than 200 nucleic acids in length. When lncRNAs are located in the nucleus, they regulate chromosome structure, participate in chromatin remodeling, and act as transcription regulators. When lncRNAs are exported to the cytoplasm, they regulate mRNA stability, regulate translation, and interfere with post-translational modification. In recent years, more and more evidences have shown that lncRNA can regulate the biological processes of tumor proliferation, apoptosis, invasion and metastasis, and can participate in a variety of tumor signaling pathways. Long-gene non-protein coding RNA641 (LINC00641), located on human chromosome 14q11.2, is differentially expressed in a variety of tumors and is related to overall survival and prognosis, etc. Interfering the expression of LINC00641 can lead to changes in tumor cell proliferation, invasion, metastasis, apoptosis and other biological behaviors. Therefore, LINC00641 is a promising new biomarker and potential clinical therapeutic target. In this review, the biological functions, related mechanisms and clinical significance of LINC00641 in many human cancers are described in detail.

In our previous study, an L1-based human papillomavirus (HPV) test using liquid-based cytology revealed that some invasive cervical cancers (ICC) exhibited multiple HPV types or harbored no HPV DNA. Here, molecular mapping of formalin-fixed paraffin-embedded cancer tissue specimens from the same patients were conducted to confirm these observations. Among 377 ICC cases, 73 eligible specimens (9 positive for multiple HPV types, 16 negative for HPV, and 48 positive for a single HPV type from the previous study) were reexamined by manual microdissection of cancer lesions, then subjected to HPV genotyping using the uniplex E6/E7 polymerase-chain-reaction method to detect all high-risk and potentially high-risk HPV types. The HPV typing results were confirmed in 52 of 73 cancer cases; among the 21 remaining cases, 15 were discordant and 6 were partially concordant. In total, 8 of 16 (50%) HPV-negative samples became positive; 6 were positive for HPV16 and 2 were positive for HPV67. Moreover, two samples previously positive for HPV6 and HPV53 were negative for HPV. All nine cancers with multiple HPV types were found to harbor only a single HPV type. In total, 63 cancer tissues exhibited a single HPV type. HPV16 and HPV18 were detected in squamous cell carcinoma (SCC) and adenocarcinoma (ADC). Alpha-5 (HPV82), -6 (HPV56), and -9 (HPV31/52/67) HPV types were detected in SCC, whereas Alpha-7 (HPV59/68) types were detected in ADC and adenosquamous carcinoma (ADSCC). These findings suggested that the different HPV types induced different histological cancers. Furthermore, all SCCs and 10 of 11 usual-type ADCs were positive for high-risk HPV types, supporting the use of HPV screening for the detection of these cancers and associated premalignant lesions. HPV16 is likely to remain undetected in some cervical cancer tissues because of low viral-copy-numbers. Putative high-risk HPV types (e.g., HPV67 and HPV82) might be high risk in Japan.

Background: The progression rate from CIN1 to CIN3 is 9.0% and that for invasive cancer is 1.0%. The large majority of CIN1 lesions regress spontaneously, and the treatment of CIN1 is still controversial.Aims: The aim of this study is to investigate the responsible HPV genotype in the low‐grade SILs, then to predict the presence of high‐grade SILs, and determine whether further treatment is needed.Methods: We use the methods of manual microdissection with FFPE tissue specimens and the E6/E7 uniplex polymerase chain reaction (PCR) to detect HPV in the lesions.Results: The HPV test was performed on 72 biopsy tissue specimens, and 55 (76.4%, 55/72) of them were HPV positive. Nine (16.4%, 9/55) of them escalated to CIN2 after LEEP or cervical conization, and 46 (83.6%, 46/55) were still CIN1. There were 17 (23.6%, 17/72) cases with HPV‐negative results in cervical biopsy tissues.HPV test of cervical biopsy diagnosed with CIN1 has a positive predictive value of 16.4% in the presence of CIN2 or higher lesions, a negative predictive value of 94.1%, a specificity of 25.8%, and a sensitivity of 90.0%. HPV test of cervical biopsy tissues for the prediction of HPV infection in LEEP or cone surgery tissues had a positive predictive value of 80.0%, a negative predictive value of 82.3%, a specificity of 56.0%, and a sensitivity of 93.6%.Conclusions: It is the first time that we have detected HPV genotype in the low‐grade SILs by the methods of manual microdissection with FFPE tissue specimens and the E6/E7 uniplex PCR. Patients with cervical biopsy tissue diagnosed with CIN1 and with a negative or only low‐risk HPV type result can be considered for follow‐up. Conversely, in cases of cervical biopsy tissue diagnosed with CIN1 positive for high‐risk HPV, surgery or a close follow‐up program can be selected.