NOB1 Expression Research Articles

Retraction Note: High Expression of RIOK2 and NOB1 Predict Human Non-small Cell Lung Cancer Outcomes

Editor's Note: this Article has been retracted; the Retraction Note is available at https://doi.org/10.1038/s41598-023-32033-5

Expression and distribution of Nob1 in the developing rat cochleae

BackgroundMammalian inner ear cells are produced during embryonic development. NIN1/RPN12 binding protein 1 homolog (Nob1), a ribosome assembly factor, is believed to be involved in transcriptional regulation and may play an important role in mediating certain physiological and pathological functions. MethodsWe investigated the expression levels and distribution patterns of Nob1 in rat cochlea at different developmental stages using reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis, and immunofluorescence microscopy (P0, P3, P7, P14, and P30, n = 11 per age group). ResultsThe expression of Nob1 was gradually upregulated from Postnatal day (P) 0 to P14 and stabilized at P30. Our results analyzing Nob1 expression at P0 and P3 in the rat cochleae revealed expression in the greater epithelial ridge cells, lesser epithelial ridge cells, and spiral ganglion neurons (SGNs), whereas low levels of Nob1 expression were observed in the stria vascularis cells. During the development of the cochlea, the organ of Corti undergoes dramatic architectural remodeling. Nob1 expression was stably detected in supporting cells and hair cells from P7 to P30, and its expression gradually increased in the SGNs. ConclusionsThus, the present study revealed that upregulation of Nob1 might explain the maturation of the cytoarchitecture in the cochlea during the postnatal period, and a complete understanding of its function in the mammalian inner ear may help to develop strategies to resolve auditory hair cell loss.

Sublethal heat treatment promotes breast cancer metastasis and its molecular mechanism revealed by quantitative proteomic analysis.

Radiofrequency ablation (RFA) is a frequently used thermal ablation technique for breast tumors. The study aimed to identify the effect of sublethal heat treatment on biological function of breast cancer cells and reveal its potential molecular mechanism. The expression profile of dysregulated proteins in sublethal heat treated breast cancer cells was analyzed by quantitative proteomic analysis. The differentially expressed proteins in the sublethal heat treated breast cancer were identified. The potential biological functions of these proteins were evaluated. The proliferation and invasion ability of breast cancer cells were enhanced after sublethal heat treatment. The expression profile of proteins in sublethal heat treated breast cancer cells was abundant, and most of which were newly discovered. A total of 206 differentially expressed proteins were identified. Among them, 101 proteins were downregulated while 105 proteins were upregulated. GO and KEGG analysis indicated that various systems were involved in the process of sublethal heat treatment including cancer, immune system, et al. Immunohistochemistry staining showed that the expression of Heat shock protein 1B, NOB1 and CRIP1 was highly expressed while the expression of BCLAF1 was lower in sublethal heat treated group. The proliferation and invasion ability of breast cancer cells were enhanced after sublethal heat treatment. Sublethal heat treatment caused gene alterations in cancer and immune system. Heat shock protein 1B, NOB1 and CRIP1 were upregulated while BCLAF1 was downregulated in breast cancer after sublethal heat treatment.

Integrated Analysis of the m6A-Related lncRNA Identified lncRNA ABALON/miR-139-3p/NOB1 Axis Was Involved in the Occurrence of Lung Cancer.

BackgroundLung cancer has the characteristics of early metastasis, high recurrence, and high mortality rate despite emerging advances in diagnostic. Early diagnosis can significantly improve the patient’s chances of cure and survival.PurposeThis study aimed to identify and assess a prognostic lncRNA/miRNA/gene signature in patients with lung cancer.MethodsPearson correlation analysis, univariate Cox analysis and LASSO Cox analysis were used to construct a lung cancer prognostic risk model based on m6A-related lncRNA. The interaction between lncRNA-miRNA-gene was verified by luciferase reporter gene experiment.ResultsThe Pearson correlation analysis determined that 1655 lncRNAs significantly correlated with the expression of m6A genes. A lung cancer prognostic risk model, including 14 m6A-related lncRNAs, was constructed through univariate Cox analysis and least absolute shrinkage and selection operator (LASSO) Cox analysis. ABALON was identified as the key lncRNA through cluster analysis and gene expression difference analysis.ConclusionIt was experimentally verified that ABALON acted as a competing endogenous RNA by sponging miR-139-3p and indirectly regulated the expression of NOB1. This study provided a new biological target for the early diagnosis of lung cancer and a new direction for studying the mechanism of lung cancer.

MicroRNA-363-3p downregulation in papillary thyroid cancer inhibits tumor progression by targeting NOB1

MicroRNA-363-3 p (miR-363–3 p) has been reported to play a crucial role in tumor development and progression, and function as a tumor suppressor in many types of cancer. In our...

Aberrant expression of miRNA-192-5p contributes to N,N-dimethylformamide-induced hepatic apoptosis.

Excessive exposure to N,N-dimethylformamide (DMF) can lead to occupational liver poisoning in workers; however, the underlying mechanism is not fully clarified. The importance of microRNAs (miRNAs) in chemical-induced hepatotoxicity has been demonstrated. To determine whether miRNAs are also involved in DMF-induced hepatotoxicity, we systematically analyzed the miRNA expression profiles in DMF-treated (75 and 150 mm) HL-7702 liver cells and controls by high-throughput sequencing. Among the altered miRNAs, miR-192-5p was the most significantly upregulated in HL-7702 cells after DMF exposure and was involved in DMF-mediated cell apoptosis. By contrast, suppression of miR-192-5p in HL-7702 cells attenuated the apoptosis induced by DMF. Furthermore, the anti-apoptotic gene (NIN1/RPN12 binding protein 1 homolog [NOB1]) was predicted to be a potential miR-192-5p target according to bioinformatics analysis. The direct interaction between miR-192-5p and NOB1 was confirmed by the dual-luciferase activity assay in HEK293FT cells. Overexpression of miR-192-5p efficiently reduced NOB1 mRNA and protein expression in HL-7702 cells. Alteration in NOB1 expression influenced DMF-induced hepatotoxicity by affecting hepatic apoptosis. In addition, the inverse correlation between miR-192-5p expression levels and NOB1 expression was further confirmed in DMF-exposed mouse liver tissue samples. These observations demonstrated that promotion of apoptosis from the suppression of NOB1 by miR-192-5p overexpression was responsible for the DMF-induced hepatotoxicity. This work provides the molecular mechanism at the miRNA level for hepatic apoptosis induced by DMF.

MiR-363 suppresses cell migration, invasion, and epithelial-mesenchymal transition of osteosarcoma by binding to NOB1

BackgroundOsteosarcoma (OS) is a primary malignant bone tumor with a high rate of metastasis and a short 5-year survival rate. MiR-363 was downregulated in a variety of tumors and played a role in suppressing tumors. However, the roles of miR-363 in osteosarcoma remain unknown; thus, the purpose of this study was to explore the functions of miR-363 in osteosarcoma.MethodsCCK-8 and transwell assays were performed to evaluate the proliferation, migration, and invasion abilities of MG63 cells. The epithelial-mesenchymal transition (EMT) and apoptosis-associated proteins were measured by using Western blot assay. Luciferase reporter assay was utilized to verify whether miR-363 directly bound to the 3′-UTR of NOB1 mRNA.ResultsMiR-363 was downregulated while NOB1 was upregulated in osteosarcoma clinical tissue specimens and cell lines as compared with the adjacent normal tissue specimens and normal cell line. The miR-363 is reversely correlated with the expression of NOB1 in osteosarcoma tissues. Overexpression of miR-363 suppressed the ability of cell migration, invasion, and EMT, whereas low expression of miR-363 promoted this ability. In addition, miR-363 inhibited osteosarcoma proliferation both in vitro and in vivo and inhibited the apoptosis in MG63 cells. Interference of NOB1 could inhibit the migration, invasion, and EMT of osteosarcoma cell line MG63. NOB1 was verified to be a direct target of miR-363 and its expression was mediated by miR-363. Re-expression of NOB1 could partially reverse the inhibitory effect of miR-363 on cell migration and invasion. In addition, low expression of miR-363 or overexpression of NOB1 predicted poor prognosis of osteosarcoma patients.ConclusionMiR-363 inhibited osteosarcoma the proliferation, migration, invasion, and EMT and induced the apoptosis by directly targeting NOB1 in MG63 cells. The newly identified miR-363/NOB1 axis provides novel insights into the pathogenesis of osteosarcoma.

Silencing NOB1 Can Affect Cell Proliferation and Apoptosis Via the C-Jun N-Terminal Kinase Pathway in Colorectal Cancer

Objectives To investigate the bio-functions and the molecular mechanisms of NIN1/proteasome 26S subunit non-ATPase 8 binding protein 1 homolog (NOB1) in colorectal cancer cells. Methods NOB1 expression was silenced using si-RNA in SW480 and LoVo cells. The transfection efficiency was measured by western blotting and RT-qPCR. Subsequently, the proliferation of SW480 and LoVo cells was determined using both MTT assay and colony-formation assay. Apoptosis and cell cycle analysis were determined using flow cytometry. Results Compared with the normal control (NC) and scramble cells, si-NOB1 could significantly attenuate the proliferation, colony-formation ability and cell percentage of S stage (p < 0.05). Additionally, at the phosphorylation level, si-NOB1 could notably increase the expression of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38. Conclusions Inhibition of NOB1 expression suppressed the proliferation, and promoted the apoptosis through regulation of the JNK signaling pathway.

MicroRNA-139-3p suppresses growth and metastasis of glioblastoma via inhibition of NIN1/RPNI2 binding protein 1 homolog.

This study aimed to investigate the role of microRNA-139-3p (miR-139-3p) in glioblastoma, and further explored the underlying molecular mechanism. Gene Expression Omnibus (GEO) dataset (accession code GSE90603) was selected to identify differentially expressed microRNAs in glioblastoma. The level of miR-139-3p in glioblastoma tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), colony formation, wound healing, and transwell invasion assays were applied to assess the role of miR-139-3p in glioblastoma cells growth and aggressiveness. The direct target of miR-139-3p was confirmed using luciferase reporter assay. NIN1/RPNI2 binding protein 1 homolog (NOB1), specific short hairpin RNA (shRNA), and lentiviral vector encoding NOB1 stable transfections were done. The expression levels of NOB1 were detected by Western blotting and qRT-PCR. Glioblastoma cells were subcutaneously implanted into nude mice to determine the role of miR-139-3p in tumor growth and metastasis in vivo. miR-139-3p was remarkably down-expressed in glioblastoma tissue compared to control normal tissue. Overexpression of miR-139-3p suppressed the growth and metastasis of glioblastoma cells. Moreover, miR-139-3p inhibited glioblastoma growth and lung metastasis in vivo, whereas under-expression of miR-139-3p caused an opposite outcome. Furthermore, our work revealed that NOB1 expression was negatively associated with miR-139-3p, and NOB1 knock-down mimicked the inhibitory effect of miR-139-3p on glioblastoma cell proliferation and mobility phenotypes. Finally, overexpression of NOB1 neutralized the inhibition of miR-139-3p in glioblastoma cells. Our findings indicated that miR-139-3p played a vital role in inhibiting glioblastoma growth and metastasis by targeting NOB1.

Long non-coding RNA ZFAS1 regulates NOB1 expression through interacting with miR-646 and promotes tumorigenesis in osteosarcoma.

Zinc finger antisense 1 (ZFAS1), a newly identified lncRNA, is aberrantly regulated in various cancers including osteosarcoma (OS). However, the underlying molecular mechanisms of ZFAS1 in OS remain to be elucidated. We used transfection, luciferase report assay, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), colony formation assay, transwell migration, invasion assays, and Western blot to determine the potential mechanisms. Our study showed that ZFAS1 was up-regulated in OS cells and promoted the colony formation, migration, and invasion of OS cells via activating the MAPK signaling pathway. Furthermore, the experimental results indicated that miR-646 was a target of ZFAS1 and there was a negative relationship between ZFAS1 and miR-646 expression. Additionally, we found that ZFAS1 in OS cells up-regulated the expression of NOB1 through sponging miR-646, finally facilitating the growth of the OS cells. These results demonstrated that ZFAS1/miR-646/NOB1 axis might play an important role in the development of OS, and ZFAS1 and miR-646 can be considered as potential biomarkers for the diagnosis and treatment of OS.

Eukaryotic translation elongation factor 1A1 positively regulates NOB1 expression to promote invasion and metastasis of hepatocellular carcinoma cells in vitro

To explore the role of eukaryotic translation elongation factor 1A1 (eEF1A1) in regulating the invasion and metastasis of hepatocellular carcinoma (HCC) cells and the possible mechanism. qRT-PCR and Western blotting were used to detect the mRNA and protein expression of eEF1A1 and NOB1 in different HCC cell lines and normal liver cells. The invasion and migration abilities of HCC cells with eEF1A1 knockdown or overexpression were examined using Transwell chamber assay and RTCA assay, and the changes in NOB1 mRNA and protein expressions in the cells were detected. The effects of increasing NOB1 expression in HCCLM3-sheEF1A1 cells and decreasing NOB1 expression in eEF1A1-overexpressing MHCC97h cells on eEF1A1 expression and cell invasion and migration abilities were analyzed using Western blotting, Transwell chamber assay and RTCA assay. The expressions of eEF1A1 and NOB1 were significantly increased in positive correlation in HCC cells as compared with normal hepatocytes. Knockdown of eEF1A1 significantly decreased the invasion and migration of HCC cells and reduced the mRNA and protein expression of NOB1 (P &lt; 0.01). Overexpression of eEF1A1 significantly enhanced invasion and migration of HCC cells and increased NOB1 mRNA and protein expressions (P &lt; 0.01). Increasing NOB1 expression in HCCLM3-sheEF1A1 cells led to the restoration of NOB1 expression and cell invasion and migration abilities (P &lt; 0.01), whereas decreasing NOB1 in MHCC97h-eEF1A1 cells resulted in inhibition of NOB1 expression and cell invasion and migration (P &lt; 0.01). eEF1A1 positively regulates the expression of NOB1 to promote the invasion and migration of HCC cells in vitro.

Effects of NOB1 on the pathogenesis of osteosarcoma and its expression on the chemosensitivity to cisplatin.

The effects of NIN1/RPN12 binding protein 1 homolog (NOB1) on the pathogenesis of osteosarcoma and its expression on the chemosensitivity to cisplatin were investigated. Seventy-four patients with osteosarcoma who received surgical resection in The Affiliated Hospital of Southwest Medical University (Sichuan, China) from September 2013 to September 2016 were enrolled in this study. The expression of NOB1 in cancer and cancer-adjacent tissues of patients was detected by reverse transcription-polymerase chain reaction, and the relationship between NOB1 expression and the pathogenesis of osteosarcoma was analyzed. The expression of NOB1 in osteosarcoma MG-63 cells was interfered with using small interfering ribonucleic acid (siRNA). Western blotting was used to detect the transfection efficiency and changes in apoptosis indicators. Cell Counting Kit-8 (CCK-8) assay was used to examine changes in the sensitivity of cells to cisplatin. The effect of NOB1 knockout on cell apoptosis was examined by flow cytometry. In patients with osteosarcoma, the level of NOB1 mRNA in cancer tissues was significantly higher than that in cancer-adjacent tissues (p<0.05), and the expression of NOB1 was correlated with Ennecking staging and tumor size (p<0.05). The expression level of the apoptotic indicator caspase-3 was activated after siRNA interfered with NOB1 expression, thus reducing the expression level of anti-apoptotic indicator B-cell lymphoma 2. CCK-8 results showed that the downregulation of NOB1 increased the sensitivity of MG-63 cells to cisplatin (p<0.05). In addition, flow cytometry showed that the downregulation of NOB1 significantly promoted the apoptosis of MG-63 cells. NOB1 is significantly upregulated in patients with osteosarcoma, thus reducing the curative effect of cisplatin chemotherapy, which indicates that the prognosis is poor.

NOB1 Gene as a Potential Biomarker in Clinical Outcomes and Prognosis of Patients with Gastric Cancer.

To investigate relationship of the Nin one binding protein (NOB1) gene with the prognosis of gastric cancer (GC). The GC tumor tissues and paired adjacent normal gastric tissues were collected from 65 patients who underwent primary gastric resection surgery in our hospital from January 2009 to July 2011. Data including age, gender, family cancer history, tumor diameter, pathological type, differentiation, clinical stage by tumor node metastasis (TNM) staging, lymphatic metastasis, and distant metastasis were collected. Expression of NOB1 and VEGF was determined using real time PCR. The relationship of NOB1 with clinical outcomes and prognosis of GC patients was analyzed by statistical methods. Both mRNA expression of NOB1 and VEGF was significantly higher in tumor tissues than that of the normal tissues, p < 0.05, and mRNA expression of NOB1 was positively correlated with mRNA expression of VEGF by Pearson's correlation analysis. Significant difference was observed in TNM stage, tumor differentiation, and metastasis between the low and high NOB1 expression groups, p < 0.05, while no significant difference was observed in age, gender, family cancer history, tumor location, and diameter. Univariate analysis showed that TNM stage, tumor differentiation, lymphatic metastasis, distant metastasis and expression of NOB1 and VEGF were all significantly different in survival and dead patients. Logistic analysis showed that NOB1 was an independent risk factor for 5-year mortality of GC patients, as well as lymphatic metastasis and distant metastasis. NOB1 was correlated with clinical outcomes and prognosis of GC patients and was an independent risk factor for 5-year mortality of GC patients. This study might provide more clinical evidences for NOB1 in GC and give a new target for diagnosis and treatment for GC patients.

Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma.

The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to participate in the deterioration of many types of cancer. However, the underlying mechanisms of SNHG1-mediating functions in osteosarcoma (OS) have yet to be elucidated. In the present study, our results showed that SNHG1 was upregulated in OS tissues and cell lines, and high SNHG1 expression predicts poor overall survival of OS patients. Knockdown of SNHG1 inhibited cell growth and metastasis of OS in vitro and in vivo. Furthermore, our data demonstrated that there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. Additionally, we identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. Collectively, these findings not only uncovered that the SNHG1/miR-326/NOB1 signaling axis has a key role in OS progression but also suggested the potential application of SNHG1 and miR-326 as biomarkers in the OS diagnosis and treatment.

MicroRNA-363 inhibits ovarian cancer progression by inhibiting NOB1.

In this study, we investigated the role of microRNA-363(miR-363) in ovarian cancer (OC) progression. MiR-363expression was downregulated in OC patient tissues and four OC cell lines (SKOV3, A2780, OVCAR and HO-8910). Low miR-363 levels were associated with advanced stage, lymph node metastasis, and poor prognosis in OC. MiR-363 overexpression decreased growth, colony formation, migration and invasiveness of SKOV3 cells. In addition, miR-363 overexpression in SKOV3 cells also decreased xenograft tumor size and weight in nude mice. Bioinformatics and dual luciferase reporter assays revealed that miR-363 suppresses expression of NIN1/RPN12 binding protein 1 homolog (NOB1) by binding to the 3’-UTR of its transcript. NOB1 expression inversely correlated with miR-363 levels in OC tissues. Thus miR-363 appears to play a tumor suppressor role in OC by inhibiting NOB1.

Low-level miR-646 in colorectal cancer inhibits cell proliferation and migration by targeting NOB1 expression.

Aberrant expression of microRNA (miRNA) is important in the progression of various human cancers, however further investigation is required in order to fully elucidate mechanisms of and validate actions of endogenous non-coding RNAs. The present study demonstrated that the expression of miR-646 was downregulated in colorectal cancer tissues and cell lines. Notably, it was observed that miR-646, a tumor suppressor, inhibited colorectal cancer cell progression through directly targeting Nin one binding protein (NOB1) expression, which possesses anti-tumor properties in colorectal cancer. Furthermore, knockdown of NOB1 expression was responsible for the tumor-suppressive effect of miR-646. The findings suggest that miR-646 may act as a therapeutic target for the treatment of colorectal cancer.

Inhibition of NOB1 by microRNA-330-5p overexpression represses cell growth of non-small cell lung cancer.

MicroRNAs (miRNAs) play critical roles in the development and progression of various cancers, including non-small-cell lung cancer (NSCLC). Studies have suggested that miR-330-5p is involved in the progression of several cancers. However, the role of miR-330-5p in NSCLC remains unclear. We investigated the effect on and mechanism of miR-330-5p in the progression of NSCLC. We found that miR-330-5p was significantly downregulated in NSCLC tissues and cell lines as detected by real-time quantitative polymerase chain reaction (RT-qPCR). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), bromodeoxyuridine (BrdU), colony formation and cell cycle assays showed that overexpression of miR-330-5p markedly inhibited cell growth. AnnexinV-FITC/PI and caspase-3 activity assays showed that overexpression of miR-330-5p significantly promoted cell apoptosis of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed NIN/RPN12 binding protein1 (NOB1) as a target gene of miR-330-5p. RT-qPCR and Western blot analysis showed that overexpression of miR-330-5p inhibited the expression of NOB1 as well as cyclinD1 and cyclin-dependent kinase4 in NSCLC cells. Moreover, overexpression of NOB1 markedly reversed the miR‑330-5p-mediated inhibitory effect on NSCLC cell growth. Correlation analysis showed that miR‑330-5p expression was inversely correlated with NOB1 mRNA expression in NSCLC tissues. Taken together, our results indicate that miR-330-5p inhibits NSCLC cell growth through downregulation of NOB1 expression. Our study suggests that miR-330-5p may serve as a potential therapeutic target for the treatment of NSCLC.

MiR-139-3p induces cell apoptosis and inhibits metastasis of cervical cancer by targeting NOB1.

MicroRNAs (miRNAs) play an important role in the development of various cancers, including cervical cancer (CC). The dysregulation of miRNA expression is associated with oncogenic transformation and miRNA often act as tumor suppressors. In this study, we aimed to analyze the effect on and mechanism of miR-139-3p in the progression of CC. The result of real-time PCR showed that miR-139-3p was down-regulated in CC tissues and cell lines. Overexpression of miR-139-3p significantly suppressed HeLa cell proliferation, migration and invasion and induced cell apoptosis. Bioinformatics analysis and luciferase reporter gene assay confirmed that NOB1 was targeted by miR-139-3p at the 3'-untranslated region (3'UTR) of its mRNA sequence. Furthermore, overexpression of NOB1 counteracted the effects of miR-139-3p suppression. Our results suggest that miR-139-3p may act as a tumor suppressor that can inhibit CC cell proliferation, migration and invasion and induce cell apoptosis through down-regulation of NOB1 expression. Taken together, this study provides a novel potential therapeutic strategy for the treatment of CC.

High Expression of RIOK2 and NOB1 Predict Human Non-small Cell Lung Cancer Outcomes.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. However, there is a shortage of suitable diagnostic markers for early stages of NSCLC, and therapeutic targets are limited. Right open reading frame (Rio) kinase 2 (RIOK2) and Nin one binding (NOB1) protein are important accessory factors in ribosome assembly and are highly expressed in malignant tumours; moreover, they interact with each other. However, the RIOK2 expression profile and its clinical significance as well as NOB1’s mechanism in NSCLC remain unknown. In this study, NSCLC cell lines and 15 NSCLC tumour tissues (paired with adjacent normal lung tissues) were collected for a real-time quantitative PCR (RT-qPCR) analysis. In addition, 153 NSCLC cases and 27 normal lung tissues were used in an immunohistochemical analysis to evaluate the RIOK2 and NOB1 expression profiles, their clinicopathological factors in NSCLC and their correlations with prognoses. RIOK2 and NOB1 were highly expressed in NSCLC cells and tissues, and their expression profiles were significantly associated with the Tumour Node Metastasis (TNM) clinical stage, lymph node metastasis, and differentiation. RIOK2 expression was correlated with NOB1. The results suggested that simultaneously determining the expression of RIOK2 and NOB1 will improve the diagnostic rate in early stages of NSCLC. Moreover, RIOK2 and NOB1 might be potential targets for NSCLC therapy.

NOB1 expression predicts early response to cisplatin-based chemotherapy in patients with advanced non-small cell lung cancer

Background: The aim of this study was to investigate the predictive value of Nin one binding (NOB1) expression for response to cisplatin-based chemotherapy in patients with advanced non-small-cell lung cancer (NSCLC).Methods: A total of 105 consecutive patients with advanced NSCLC were retrospectively investigated between January 2012 and June 2014. We used transbronchial biopsy to collect cancer tissue samples. Immunohistochemistry were used in the detection of NOB1 protein expression. We assessed the chemotherapy early response by response evaluation criteria in solid tumours (RECIST) Version 1.1 at the end of the second cycle of chemotherapy.Results: In the 105 transbronchial biopsy NSCLC specimens, 22 (21.0%) stained NOB1 − , 35 (33.3%) stained +, 31 (29.5%) stained ++ and 17 (16.2%) stained +++. The early response rate to chemotherapy was 59.0% in overall NSCLC. Early response to chemotherapy has no relationship with patients' age, gender, smoke status, performance status and chemotherapy regimens (P>0.05), but related with TMN stage, histopathological grade, as well as NOB1 expression (P < 0.05). In squamous cell carcinoma and non-squamous cell carcinoma, same results were found. Logistic regression analysis showed TMN stage, histopathological grade and NOB1 expression were independent prognosis factors for early response to cisplatin-based chemotherapy in patients with advanced NSCLC. After adjusted by TMN stage and histopathological grade, the OR for NOB1 expression was 1.429 (95% CI 1.115–1.743, P = 0.008) for early response to chemotherapy.Conclusion: Our results suggest that enhanced expression of NOB1 related with poor early response to cisplatin-based chemotherapy in patients with advanced non-small cell lung cancer.