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Induction Of XLF And 53BP1 Expression Is Associated With Temozolomide Resistance In Glioblastoma Cells.

Glioblastoma (GBM) is the most commonly diagnosed primary brain tumor in adults. The 14.6 months median survival period of GBM patients is still palliative due to resistance to the first-line chemotherapeutic agent temozolomide (TMZ).

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LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.

Lung cancer is a malignant tumor with extremely high morbidity and mortality. Recent studies have identified the vital role of LINC00511 (lncRNAs) in the development and progression of non-small cell lung cancer (NSCLC). In this research, we aim to explore the biological function of LINC00511 in the development and metastasis of NSCLC.

1100 related Products with: LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.

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CircRNA UBAP2 promotes the progression of ovarian cancer by sponging microRNA-144.

This study aims to elucidate the regulatory effect of circular RNA UBAP2 (circUBAP2) on the progression of ovarian cancer (OC).

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TMPO-AS1 promotes cervical cancer progression by upregulating RAB14 via sponging miR-577.

Accumulating evidence has shown that long non-coding RNAs play a key role in cancer initiation and development. However, the effect of TMPO antisense RNA 1 (TMPO-AS1) on the progression of cervical cancer (CC) remains to be determined.

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IGF2-AS affects the prognosis and metastasis of gastric adenocarcinoma via acting as a ceRNA of miR-503 to regulate SHOX2.

Disorder of long non-coding RNAs (LncRNAs) is found in various types of cancers and demonstrated to be associated with tumor occurrence and development. Our study found that lncRNA insulin growth factor 2 antisense (IGF2-AS) is up-regulated in gastric adenocarcinoma (GAC) tissues and correlated with poor prognosis in patients with GAC. Cell counting kit-8 (CCK8), colony formation, wound healing and transwell assays revealed that knockdown of IGF2-AS in BGC823 and SGC7901 cells significantly suppressed cell proliferation, migration and invasion. While, overexpression of IGF2-AS in AGS and MGC803 cells exhibited the opposite effects. RNA-FISH and subcellular fractionation assay found that most IGF2-AS was distributed in the cytoplasm, suggesting that IGF2-AS functioned as a potential ceRNA. RNA binding protein immunoprecipitation (RIP) assays further confirmed this assumption. By informatics prediction and luciferase reporter assay, we found that IGF2-AS functioned as an efficient miR-503 sponge and the level of miR-503 showed an inverse correlation with IGF2-AS. Short stature homeobox 2 (SHOX2) is predicted and verified as a target of miR-503. Moreover, IGF2-AS expression exhibited a negative correlation with miR-503 and a positive correlation with IGF2-AS. Subsequent rescue assay revealed that down-regulation of miR-503 or restoration of SHOX2 canceled IGF2-AS depletion-induced depression in proliferation and motility of BGC823 and SGC7901 cells. Meanwhile, up-regulation of miR-503 or down-regulation of SHOX2 decreased IGF2-AS overexpression induced promotion in proliferation and motility of AGS and MGC803 cells. In vivo tumorigenicity assay showed that knockdown of IGF2-AS significantly reduced tumor volume. Taken together, our results demonstrated that IGF2-AS takes important regulatory parts in GAC development by functioning as a ceRNA to regulate SHOX2 via sponging miR-503.

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Low expression of lncRNA NBAT-1 promotes gastric cancer development and is associated with poor prognosis.

This study aimed to investigate the regulatory effect of long non-coding RNA (lncRNA) NBAT-1 (neuroblastoma associated transcript 1) on the development and prognosis of gastric cancer (GC), and its underlying mechanism.

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CD73 promotes hepatocellular carcinoma progression and metastasis via activating PI3K/AKT signaling by inducing Rap1-mediated membrane localization of P110β and predicts poor prognosis.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide because of rapid progression and high incidence of metastasis or recurrence. Accumulating evidence shows that CD73-expressing tumor cell is implicated in development of several types of cancer. However, the role of CD73 in HCC cell has not been systematically investigated and its underlying mechanism remains elusive.

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Downregulated lncRNA ADAMTS9-AS2 in breast cancer enhances tamoxifen resistance by activating microRNA-130a-5p.

The aim of this study was to elucidate the regulatory effect of long non-coding RNA (lncRNA) ADAMTS9-AS2 on Tamoxifen (TAM) resistance in breast cancer (BC), and to explore its underlying mechanism.

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UV-Radiation Response Proteins Reveal Undifferentiated Cutaneous Interfollicular Melanocytes with Hyperradiosensitivity to Differentiation at 0.05 Gy Radiotherapy Dose Fractions.

To date, the response activated in melanocytes by repeated genotoxic insults from radiotherapy has not been explored. We hypothesized that the molecular pathways involved in the response of melanocytes to ionizing radiation and ultraviolet radiation (UVR) are similar. Skin punch biopsies, not sun-exposed, were collected from prostate cancer patients before, as well as at 1 and 6.5 weeks after daily doses of 0.05-1.1 Gy. Interfollicular melanocytes were identified by ΔNp63- and eosin-periodic acid Schiff staining. Immunohistochemistry and immunofluorescence were performed to detect molecular markers of the melanocyte lineage. Melanocytes were negative for ΔNp63, and the number remained unchanged over the treatment period. At radiation doses as low as 0.05 Gy, melanocytes express higher protein levels of microphthalmia-associated transcription factor (MITF) and Bcl-2. Subsets of MITF- and Bcl-2-negative melanocytes were identified among interfollicular melanocytes in unexposed skin; the cell number in both subsets was reduced after irradiation in a way that indicates low-dose hyperradiosensitivity. A corresponding increase in MITF- and Bcl-2-positive cells was observed. PAX3 and SOX10 co-localized to some extent with MITF in unexposed skin, more so with radiation exposure. Low doses of ionizing radiation also intensified c-KIT and DCT staining. Nuclear p53 and p21 were undetectable in melanocytes. Apoptosis and proliferation could not be observed. In conclusion, undifferentiated interfollicular melanocytes were identified, and responded with differentiation in a hypersensitive manner at 0.05 Gy doses. Radioresistance regarding cell death was maintained up to fractionated doses of 1.1 Gy, applied for 7 weeks. The results suggest that the initial steps of melanin synthesis are common to ionizing radiation and UVR, and underline the importance of keratinocyte-melanocyte interaction behind hyperpigmentation and depigmentation to radiotherapy.

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