MIR100HG, also known as lncRNA mir-100-let-7a-2-mir-125b-1 cluster host gene, is a new and critical regulator in cancers in recent years. MIR100HG is dysregulated in various cancers and plays an oncogenic or tumor-suppressive role, which participates in many tumor cell biology processes and cancer-related pathways. The errant expression of MIR100HG has inspired people to investigate the function of MIR100HG and its diagnostic and therapeutic potential in cancers. Many studies have indicated that dysregulated expression of MIR100HG is markedly correlated with poor prognosis and clinicopathological features. In this review, we will highlight the characteristics and introduce the role of MIR100HG in different cancers, and summarize the molecular mechanism, pathways, chemoresistance, and current research progress of MIR100HG in cancers. Furthermore, some open questions in this rapidly advancing field are proposed. These updates clarify our understanding of MIR100HG in cancers, which may pave the way for the application of MIR100HG-targeting approaches in future cancer diagnosis, prognosis, and therapy.

BGN belongs to class of small leucine rich proteoglycans, which is high expression in plenty of human cancers. However, the detailed role of BGN remains unclear in Head and neck squamous cell carcinoma (HNSC). In this study, we assessed the transcriptional expression, protein expression, prognosis, co-expressed genes, functional enrichment, and hub genes in HNSC patients based on the data published in the following databases: ONCOMINE, GEPIA, GEO, LinkedOmics, and HPA databases. Data from the TCGA database was used to analyze the correlations between BGN expression and different clinicopathological features, as well as prognostic analysis. We found that the expression of BGN is higher in patients with HNSC than in control tissues. Pathologically, high BGN expression was significantly correlated with T3 and T4 stage. Besides, high expression of BGN is a poor prognostic factor for overall surviva, not disease free survival. The co-expression genes associated with BGN expression exhibited enriched in various function and pathway, such as extracellular matrix, mitochondrion, PI3K-Akt signaling pathway. A total of 10 hub genes were identified from the co-expressed genes, within which five genes, including FSTL1, LAMB1, SDC2, VCAN, and IGFBP7, were significantly increased in patient's with HNSC. BGN exhibited weak correlations with tumor-infiltrating CD4+ T, macrophages cell, and dendritic cells. Futhermore, many markers of infiltrating immune cells, such as Treg, showed different BGN-related immune infiltration patterns. BGN expression showed strong correlations with diverse immune marker sets in COAD and STAD. Our results demonstrated that BGN is high expression in HNSC and is a poor prognostic factor for clinical outcome in patients with HNSC. It could serve as a potential prognostic biomarker for patients survival in HNSC.

Transcription factors Sox2 and Oct4 are essential in maintaining the pluripotency of embryonic stem cells and conferring stemness in cancer stem-like (CSL) cells. SORE6, an in-vitro reporter system, was designed to quantify the transcription activity of Sox2/Oct4 and identify CSL cells in non-hematologic cancers. Using SORE6, we identified and enriched CSL cells in ALK-positive anaplastic large cell lymphoma (ALK + ALCL). Two ALK + ALCL cell lines, SupM2 and UCONN-L2, contained approximately 20% of SORE6+ cells, which were purified based on their expression of green fluorescent protein. We then performed functional studies using single-cell clones derived from SORE6− and SORE6+ cells. Compared to SORE6− cells, SORE6+ cells were significantly more chemoresistant and clonogenic in colony-formation assays. Sox2/Oct4 are directly involved in conferring these CSL properties, since the shRNA knockdown of Sox2 in SORE6+ significantly lowered their chemoresistance, while enforced expression of Sox2/Oct4 in SORE6− cells produced opposite effects. Using Western blots, we found that the expression and subcellular localization of Sox2/Oct4 were similar between SORE6− and SORE6+ cells. However, in SORE6+ but not SORE6− cells, Sox2 and Oct4 abundantly bound to a probe containing the SORE6 consensus sequence. c-Myc, previously shown to regulate cancer stemness in ALK + ALCL, regulated the SORE6 activity. In conclusion, SORE6 is useful in identifying/enriching CSL cells in ALK + ALCL.

The expression of NKG2D ligands (NKG2DLs), induced by stress or malignant transformation, is considered to mark dysfunctional cells for elimination by NK cells or cytotoxic lymphocytes via NKG2D/NKG2DLs pathway. ULBP1, ULBP2, and ULBP3 (ULBP1-3), three members of NKG2DLs, are common expressed in breast cancer. We analyzed the expression of ULBP1-3 in breast cancer and healthy control tissues with several databases, and found that breast cancer had a higher mRNA level of ULBP1 and ULBP2, and a higher protein level of ULBP1-3. Analysis with the bc-GenExMiner database showed that the expression of ULBP1-3 were down-regulated by the wild type P53, PR, and HER2+ in breast cancer. Except for ULBP1, ULBP2 and ULBP3 were associated with poor prognosis in breast cancer. The analysis of the correlated genes suggested that ULBP1-3 have some common pathways including NK cell-mediated cytotoxicity, microRNA in cancer, and IL-17 signaling pathway, whereas they also have their own pathways. But ULBP1-3 expression were also a significantly negative correlation with few immune markers on NK and central memory CD8+ T. The correlations and co-occurrence between ULBP1-3 and the other ligands by using TIMER and cbioportal databases showed the same form proteins or the proteins in the same family were more likely to change at the same time. Together with all these findings, increased ULBP2 and ULBP3 were correlated with poor prognosis and various markers on immune cells. These conclusions indicated that ULBP2 and ULBP3 could serve as potential biomarkers to assess prognosis and they were strong correlation with various markers in immune cells.