Long noncoding RNAs (lncRNA) are increasingly implicated in oncogenesis. Here, it is determined that / is upregulated in glioblastoma multiforme (GBM) and aggressive wild-type IDH1/2 grade 2/3 gliomas and upregulation associates with poor patient outcomes. is similarly upregulated in over 10 other cancer types and associates with a poor prognosis in 7 other cancer types. Inhibition of the mostly cytoplasmic decreases, and overexpression increases cellular invasion. knockdown alters the transcription of genes important to epithelial-to-mesenchymal transition (EMT). PARIS and Ribo-seq data, together with secondary structure prediction, identified a protein-bound 121-bp stem-loop structure at the 3' end of whose overexpression is sufficient to increase invasion of GBM cells. Point mutations in the stem-loop suggest that stem formation in the hairpin is essential for function. has a nearly identical homolog, , which encodes a near identical hairpin, is equally expressed in low-grade glioma (LGG) and GBM, predicts poor patient survival in these tumors, and is also reduced by knockdown. Together, these data reveal that and its homolog associate with aggressive tumors and promote cellular invasion through a mechanism that requires the structural integrity of a hairpin structure. Frequent upregulation of the lncRNA, , in glioblastoma and other tumor types combined with its prognostic potential and ability to promote invasion suggests as a potential biomarker and therapeutic target. .

Despite significant advances in the treatment of head and neck squamous cell carcinoma (HNSCC), the survival rate has not changed in the last decades. Therefore, the development of novel therapeutic strategies is pursued. Cancer-testis antigens (CTA) are strong immunogenic proteins with a tumor-restricted expression pattern, and are considered ideal targets for tumorspecific immunotherapeutic approaches. In this study, using an in silico approach, we selected, among 139 previously described CTA, candidates to be evaluated in 89 HNSCC and 20 normal mucosa samples. SPANX-CD (71.9%), MAGEB2 (44.9%), MAGEA1 (44.9%), MAGEB6 (32.6%), and CXORF48 (27.0%) were found frequently expressed in HNSCC, and over 85% of the tumors expressed at least one of these five CTAs. The mRNA positivity of CXORF48, MAGEB6, and CRISP2 presented significant associations with recognized clinical features for poor outcome. Furthermore, MAGEA3/6 positivity was associated with significantly better disease-free survival (DFS, P ¼ 0.014), and the expression of this antigen was shown to be an independent prognostic factor for tumor recurrence. In conclusion, one of five selected CTAs is expressed in at least 85% of the HNSCCs, suggesting a possible usage as target for immunotherapeutic approaches, and the mRNA-positivity for MAGEA3/ 6 is shown to be an independent marker for DFS. Mol Cancer Ther; 14(3); 828-34. Ó2015 AACR.

These findings suggest GAGE1 and XAGE1 expressions to be useful as prognostic markers for HNSCC.

Despite the advancements in cancer treatments, gastric cancer is still one of the leading causes of death worldwide. In this context, it is of great interest to discover new and more effective ways of treating this disease. Accumulated evidences have demonstrated the amplification of 8q24.21 region in gastric tumors. Furthermore, this is the region where the widely known MYC oncogene and different microRNAs are located. MYC deregulation is key in tumorigenesis in various types of tissues, once it is associated with cell proliferation, survival, and drug resistance. microRNAs are a class of noncoding RNAs that negatively regulate the protein translation, and which deregulation is related with gastric cancer development. However, little is understood about the interactions between microRNAs and MYC. Here, we overview the MYC role and its relationship with the microRNAs network in gastric cancer aiming to identify potential targets useful to be used in clinic, not only as biomarkers, but also as molecules for development of promising therapies.

Gastric cancer is one of the most common cancers and the third cause of cancer-related death worldwide. The treatment of GC patients improved due to advancements in surgery, radiotherapy and chemotherapy. However, the long-term survival rate of patients with gastric cancer remains around 20%. Thus, development of novel therapeutic approaches is of great interest, in order to reduce the need for mutilating surgeries and morbid adjuvant therapies. For many years, it was believed that the RNA was a mere intermediate molecule in the genetic information flow. However, during the past decades, with the advent of new sequencing technologies, it was revealed that non-coding RNAs play important roles in many different biological processes. The Wnt/β-catenin signaling pathway has been reported to regulate crucial events during neoplasic development, such as cell differentiation, proliferation, invasion, migration, apoptosis, and angiogenesis. In this review, we will focus on microRNAs and long non-coding RNAs that have been implicated in gastric cancer tumorigenesis via modulation of the Wnt/β-catenin signaling pathway, which provided some biomarkers to prognosis, diagnosis, and therapy.

Gastric cancer is the subject of clinical and basic studies due to its high incidence and mortality rates worldwide. Due to the diagnosis occurring in advanced stages and the classic treatment methodologies such as gastrectomy and chemotherapy, they are extremely aggressive and limit the quality of life of these patients. CRISPR/Cas9 is a tool that allows gene editing and has been used to explore the functions of genes related to gastric cancer, in addition to being used in the treatment of this neoplasm, greatly increasing our understanding of cancer genomics. In this mini-review, we seek the current status of the CRISPR/Cas9 gene-editing technology in gastric cancer research and clinical research.

<p>Expression of genes involved in EMT are decreased by si LINC00152 rescued by LINC00152 m8 overexpression. A-G) qRT-PCR showing (A) LINC00152, (B) TPM2, (C) PTX3, (D) IGFBP4, (E) TGM2, (F) SPP1, (G) LUM expression after siGL2 and pcDNA3, or siLINC00152_II and pcDNA3, or siLINC00152_II and LINC00152 m8 transfections.</p>

<p>A protein-bound stem loop in LINC00152. A and B) The two lowest free-energy structures of LINC00152, predicted by mfold. Boxed areas show overlapping stem-loop regions between the structures which also overlaps with the PARIS reads and Ribo-seq reads. C) IGV view of PARIS reads (two separate experiments) generated from HeLa cells. The boxed areas overlap with the beige area in A. The darker shaded areas show the reads obtained from PARIS with 2-bp gap where indicated. D) Top three tracks: IGV view of Ribo-seq reads from the brain showing sites bound by RNPs as darker shaded areas in the top five tracks. Boxed area is the same as the boxed area in A. Bottom three tracks: RNA-seq reads from the brain that map to exon 2 of LINC00152. The different tracks represent three biological samples. If there is >20% of reads at a position is different from the reference genome (due to mutation, polymorphism, cross-link site), the nucleotide is colored as follows: A: green; T: red; C: blue; G: orange.</p>