lncRNA AWPPH Research Articles

The emerging role of LncRNA AWPPH in multiple cancers: a review study.

Long non-coding RNAs (lncRNAs) are transcribed RNA molecules longer than 200 nucleotides in length that have no protein-coding potential. They are able to react with DNA, RNA, and protein. Hence they involve in regulating gene expression at the epigenetic, transcriptional, post-transcriptional, and translational levels. LncRNAs have been proven to play an important role in human malignancies and prognostic outcomes. In this review, we will comprehensively and functionally discuss the role of a novel identified lncRNA, namely lncRNA WAPPH located on human chromosome 2q13, in various cancers. Increasing research studies have shown that lncRNA AWPPH is deregulated in different malignancies, including breast cancer, gastric cancer, colorectal cancer, ovarian cancer, bladder cancer, leukemia, and others. LncRNA WAPPH serves as an oncogene in tumorigenesis and the development of cancer. Moreover, lncRNA AWPPH is involved in numerous biological processes of solid and blood cancers. Taken together, based on our scrutiny analysis, lncRNA AWPPH can be regarded as a putative biomarker for diagnosis or therapeutic target in human malignancies.

Retraction: LncRNA AWPPH promotes the growth of triple-negative breast cancer by up-regulating frizzled homolog 7 (FZD7).

This article is being retracted from Bioscience Reports at the request of the authors. Further experiments performed by the authors showed that LncRNA AWPPH had no promotion of cell growth in HCC38, HCC1187 or 4T1. Thus, the conclusion that LncRNA AWPPH is a tumor promoter in TNBC should be further studied to validate the results.The Editor-in-Chief and Editorial Board agree with the retraction.

Retraction.

Retraction: "LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression," by Feng Zhu, Xinjun Zhang, Qinnan Yu, Guangye Han, Fengxia Diao, Chunlei Wu, Yan Zhang, J Cell Biochem. 2018; 4496-4505: The above article, published online on 12 December 2017 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.26556), has been retracted by agreement between the the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction.

LncRNA AWPPH as a prognostic predictor in human cancers in Chinese population: evidence from meta-analysis.

Background: Long non-coding RNA associated with poor prognosis of hepatocellular carcinoma (AWPPH) is dysregulated in a variety of human cancers. However, the prognostic value of AWPPH in various cancers remains unclear.Methods: Comprehensive literature search was performed in PubMed, Web of Science, CNKI and Wangfang databases, and eligible studies were obtained according to the inclusion and exclusion criteria. The pooled hazard ratios (HRs) and odds ratios (ORs) were applied to assess the clinical value of AWPPH expression for overall survival (OS) and clinicopathological features.Results: A total of 19 articles including 1699 cancer patients were included in the study. The pooled results demonstrated that evaluated AWPPH expression was positively related to a poorer overall survival of patients with cancers (HR = 1.79, 95%CI: 1.44–2.14, P<0.001). Subgroup analysis revealed that tumor type and sample size affect the predictive value of AWPPH on OS, whereas cut-off value and HR estimation method have no impact on it. In addition, the pooled data also showed that AWPPH was positively linked to advanced TNM stage (OR = 2.50, 95%CI: 1.94–3.22, P<0.001), bigger tumor size (OR = 2.64, 95%CI: 1.47–4.73, P=0.001), macro-vascular invasion (OR = 2.08, 95%CI: 1.04–4.16, P=0.04) and lymph node metastasis (OR = 2.68, 95%CI: 1.82–3.96, P<0.001). Moreover, the results of the trim and fill analysis confirmed the reliability of our finding.Conclusions: Up-regulation of AWPPH was associated with advanced TNM stage, bigger tumor size, worse lymph node metastasis, macro-vascular invasion and shorter overall survival, suggesting that AWPPH may serve as a biomarker for prognosis and clinicopathological characteristics in human cancers among the Chinese population.

Long non‑coding RNA AWPPH interacts with ROCK2 and regulates the proliferation and apoptosis of cancer cells in pediatric T‑cell acute lymphoblastic leukemia

The long non-coding (lnc)RNA associated with poor prognosis of hepatocellular carcinoma (AWPPH) serves as an oncogene in several cancers, such as liver and bladder cancers, however, to the best of our knowledge, its function in T-cell acute lymphoblastic leukemia is unknown. The results of the present study revealed that the expression levels of lncRNA AWPPH and Rho-associated protein kinase 2 (ROCK2) were upregulated in the bone marrow of patients with pediatric T-cell acute lymphoblastic leukemia compared with healthy controls. Expression levels of lncRNA AWPPH and ROCK2 were positively correlated with each other. lncRNA AWPPH and ROCK2 overexpression promoted the proliferation and inhibited the apoptosis of Loucy cells, an acute lymphoblastic leukemia cell line. Overexpression of lncRNA AWPPH resulted in upregulation of ROCK2 expression in Loucy cells. Similarly, ROCK2 overexpression also resulted in upregulation of lncRNA AWPPH in Loucy cells, suggesting an element of reciprocity in the function of lncRNA AWPPH and ROCK2. It was concluded that lncRNA AWPPH promoted the proliferation and inhibited the apoptosis of cancer cells in pediatric T-cell acute lymphoblastic leukemia possibly through interactions with ROCK2.

Long non-coding RNA AWPPH enhances malignant phenotypes in nasopharyngeal carcinoma via silencing PTEN through interacting with LSD1 and EZH2.

Evidence has emerged identifying long noncoding RNAs (lncRNAs) as important regulators of various cancers including nasopharyngeal carcinoma (NPC). LncRNA AWPPH is an oncogene recently identified in several cancers. However, the underlying role of AWPPH in NPC is still unclear and thus worth exploring. In this study, AWPPH expression was markedly upregulated in NPC cells. Further, loss- and gain-of-function assays indicated that AWPPH facilitates cell proliferation and migration and hinders apoptosis in NPC cells. Moreover, cytoplasmic AWPPH was predicted to share a common RNA-binding protein, IGF2BP1, with LSD1. The interaction between IGF2BP1 and both AWPPH and LSD1 mRNA was verified in NPC cells, and AWPPH stabilized LSD1 mRNA to enhance the expression of LSD1 in NPC through such interactions. Furthermore, nuclear AWPPH repressed PTEN expression through recruiting EZH2 and LSD1 to the PTEN promoter in NPC cells. Final rescue assays demonstrated that silenced PTEN could reverse the suppressive influence of AWPPH depletion on the progression of NPC. Collectively, our study shows that AWPPH inhibits PTEN expression to drive NPC progression through interacting with LSD1 and EZH2, providing potential biomarkers for NPC treatment.

LncRNA AWPPH is downregulated in osteoporosis and regulates type I collagen α1 and α2 ratio

Normal ratio of type I collagen α1 to α2 (2:1) maintains normal bone microarchitecture. Altered ratios lead to formation of collagen homotrimers and deteriorated bone microarchitecture. In this study, we aimed to investigate the role of lncRNA AWPPH in osteoporosis. We observed that the expression of lncRNA AWPPH was downregulated in osteoporosis patients than that in healthy controls. Downregulated expression of lncRNA AWPPH distinguished osteoporosis patients from healthy controls. In vitro cell experiments showed that knockdown of lncRNA AWPPH led to upregulated α1 but downregulated expression of α2 in osteoblasts, which made the α1 to α2 ratio higher than 2:1. In contrast, overexpression of lncRNA AWPPH led to downregulated α1 but upregulated α2 in osteoblasts, which made the α1 to α2 ratio lower than 2:1. Therefore, lncRNA AWPPH is downregulated in osteoporosis and altered the expression of lncRNA AWPPH regulates type I collagen α1 and α2 ratio in osteoblasts.

LncRNA AWPPH accelerates the progression of non-small cell lung cancer by sponging miRNA-204 to upregulate CDK6.

This study aims to uncover the function of long non-coding RNA (lncRNA) AWPPH in the progression of non-small cell lung cancer (NSCLC) and the potential mechanism. AWPPH and microRNA (miRNA-204) levels in NSCLC tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Kaplan-Meier curves were introduced for assessing overall survival in NSCLC patients expressing high or low level of AWPPH. Potential correlation between expression levels of AWPPH and miRNA-204 in NSCLC tissues was analyzed by Spearman correlation test. Through Dual-Luciferase reporter gene assay, the interaction among AWPPH, miRNA-204, and CDK6 was identified. Potential impacts of AWPPH/miRNA-204/CDK6 regulatory loop on mediating proliferative, migratory, and invasive capacities of A549 cells were evaluated through cell counting kit-8 (CCK-8) and transwell assay. Upregulated AWPPH and downregulated miRNA-204 were determined in NSCLC tissues. AWPPH level was negatively correlated to overall survival in NSCLC patients and miRNA-204 level in NSCLC tissues. Silence of AWPPH attenuated proliferative, migratory, and invasive capacities in A549 cells. MiRNA-204 was the downstream gene of AWPPH. Knockdown of miRNA-204 reversed the decreased viability, migratory, and invasive rates in A549 cells with AWPPH knockdown. In addition, CDK6 was the target gene of miRNA-204. Overexpression of miRNA-204 downregulated CDK6 level in A549 cells. The attenuated proliferative, migratory, and invasive capacities in A549 cells overexpressing miRNA-204 were reversed after CDK6 overexpression. LncRNA AWPPH serves as the miRNA-204 sponge to upregulate CDK6 level, thus aggravating the progression of NSCLC.

LncRNA AWPPH participates in the development of non-traumatic osteonecrosis of femoral head by upregulating Runx2.

AWPPH is a newly discovered long noncoding (lnc)RNA that plays an oncogenic role in development of several types of malignancies, whiles its involvement in non-traumatic osteonecrosis of femoral head (ONFH) is unknown. Therefore, the present study aimed to investigate the functionality of AWPPH in non-traumatic ONFH. Blood and mesenchymal stem cells (MSCs) were obtained from both non-traumatic ONFH patients and healthy controls, and expression of AWPPH in those tissues was detected by RT-qPCR. Receiver operating characteristic curve analysis was performed to investigate the diagnostic value of lncRNA AWPPH expression for non-traumatic ONFH. Bone morphogenic protein (BMP-2) was used to treat MSCs to induce osteogenic differentiation and the effects on lncRNA AWPPH expression was detected by RT-qPCR. LncRNA AWPPH overexpression and short hairpin (sh)RNA silencing cell lines were established and the effects on runt-related transcription factor 2 (Runx2) expression were detected by western blotting. It was demonstrated that AWPPH was significantly downregulated in non-traumatic ONFH patients compared with in healthy controls in both MSCs and serum. Expression of AWPPH in MSCs and serum is a sensitive diagnostic marker for non-traumatic ONFH. Expression of AWPPH exhibited no significant correlation with patients' age, gender and living habits, but was significantly correlated with course of disease. BMP-2 treatment significantly increased the expression level of AWPPH in human MSCs from bone marrow (hMSC-BM). AWPPH overexpression promoted, while AWPPH short hairpin RNA silencing inhibited the expression of Runx2 expression in hMSC-BM cells. Therefore, it was concluded that lncRNA AWPPH may participate in the development of ONFH by upregulating Runx2.

LncRNA AWPPH promotes the invasion and migration of glioma cells through the upregulation of HIF1α.

Long non-coding RNA (lncRNA) AWPPH has been revealed to serve pivotal roles in bladder cancer and liver cancer. The aim of the present study was to determine the involvement of lncRNA AWPPH in glioma. It was observed in the present study that the expression levels of AWPPH in plasma were significantly higher in patients with metastatic glioma compared with those in patients with non-metastatic glioma and healthy controls. In effect, overexpression of AWPPH allowed the differentiation of patients with metastatic glioma from patients with non-metastatic glioma and in healthy controls. Increased migration and invasion rates of glioma cells and upregulated hypoxia-inducible factor 1-α (HIF1α) expression were observed following AWPPH overexpression. HIF1α overexpression exhibited no significant effects on AWPPH expression but also promoted the migration and invasion of cancer cells. HIF1α small interfering RNA silencing attenuated the enhancing effects of AWPPH overexpression on the migration and invasion of glioma cells. From the results of the present study it was concluded that AWPPH may promote glioma metastasis by serving as an upstream activator of HIF1α.

LncRNA AWPPH promotes the migration and invasion of glioma cells by activating the TGF-β pathway.

The long noncoding RNA (lncRNA) AWPPH, also termed microRNA-4435-2HG, has been associated with the poor prognosis of patients with hepatocellular carcinoma (HCC), and has been demonstrated to promote the progression of HCC and bladder cancer. The present study aimed to investigate the role of lncRNA AWPPH in glioma. The expression levels of AWPPH in tumor tissues obtained from patients with glioma and in plasma samples obtained from patients with glioma and healthy controls were detected by reverse transcription-quantitative polymerase chain reaction. The plasma levels of transforming growth factor (TGF)-β1 were measured by an enzyme-linked immunosorbent assay. An AWPPH expression vector was transfected into human glioma cell lines. Subsequently, cancer cell migration and invasion were assessed by Transwell migration and invasion assays, respectively. The expression of TGF-β1 in the transfected-glioma cells was detected by western blot analysis. It was identified that AWPPH expression levels in tumor tissues were higher in patients with metastatic glioma; however, no significant differences in AWPPH expression were revealed between patients with different tumor sizes. The plasma levels of AWPPH were positively correlated with the plasma levels of TGF-β1 in patients with glioma but not in healthy controls. In addition, AWPPH overexpression enhanced cancer cell migration and invasion, and upregulated TGF-β1 expression. Treatment with TGF-β1 demonstrated no significant effect on AWPPH expression; however, a TGF-β inhibitor attenuated the effects of AWPPH overexpression on cell migration and invasion. Therefore, the present study proposed that AWPPH may promote the migration and invasion of glioma cells by activating the TGF-β pathway.

Inhibition of long non-coding RNA-AWPPH decreases osteosarcoma cell proliferation, migration and invasion.

Long non-coding RNAs (lncRNAs) serve a crucial role in various types of cancer. The lncRNA AWPPH has been reported to promote hepatocellular carcinoma and bladder cancer progression. However, to the best of our knowledge, the biological roles of AWPPH in osteosarcoma (OS) remain unclear. In the present study, the levels of AWPPH in OS tissues and cell lines were determined by reverse transcription-quantitative polymerase chain reaction. An MTT assay was used to detect OS cell proliferation. The levels of proteins associated with the PI3K/Akt signaling pathway and apoptosis were determined by western blotting. Wound-healing and Transwell assays were conducted to determine cell migration and invasion, respectively. The results demonstrated that AWPPH was highly expressed in OS tissues and cells. Functional analyses revealed that AWPPH depletion significantly inhibited OS cell proliferation and migration, and promoted OS cell apoptosis. Furthermore, AWPPH downregulation significantly inhibited the PI3K/AKT pathway. The present study demonstrated that AWPPH was highly expressed in OS, and that AWPPH promoted OS cell proliferation and migration, and inhibited OS cell apoptosis, which may be mediated by PI3K/AKT pathway activation.

Up-regulation of long non-coding RNA AWPPH inhibits proliferation and invasion of gastric cancer cells via miR-203a/DKK2 axis.

AWPPH is a newly discovered long non-coding RNA (lncRNA). However, the expression and function of AWPPH in gastric cancer (GC) have not yet been clarified. This study tries to assess the expression and biological roles of AWPPH in GC and the underlying mechanism. The expression of lncRNA AWPPH was evaluated in GC tissues and adjacent normal tissues from 40 patients. Cell Counting Kit-8 (CCK8) and transwell assays were applied to assess cell proliferation and invasion capabilities. Bioinformatics tool was employed to predict AWPPH's sponging miRNA, while luciferase reporter assays were used to verify the target. LncRNA AWPPH was remarkably downregulated in GC and associated with metastasis. CCK8 and transwell assays proved that AWPPH inhibited cell proliferation and invasion in GC cells. MiR-203a was a predicted and further verified target of AWPPH. DKK2 was verified as a direct target of miR-203a. Upregulation of miR-203a attenuated the repressive effects of AWPPH on GC cell proliferation and invasion. AWPPH inhibited GC cell proliferation and invasion via miR-203a/DKK2 axis. This finding might provide new insight for the potential therapeutic strategies for GC in the future.

LncRNA AWPPH participates in the metastasis of non-small cell lung cancer by upregulating TGF-β1 expression.

Long non-coding RNA (lncRNA) AWPPH is a characterized oncogenic lncRNA in hepatocellular carcinoma and bladder cancer. The aim of the present study was to investigate the potential involvement of AWPPH in non-small cell lung cancer (NSCLC). Expression of AWPPH in lung biopsy tissues and serum of both healthy controls and patients with NSCLC with different tumor sizes, and with and without distant tumor metastasis was detected by reverse transcription-quantitative PCR. AWPPH expression vector was constructed and transfected into cells of human NSCLC cell lines. Expression of TGF-β1 was detected by western blot analysis. Cell migration and invasion were detected by Transwell migration and invasion assay. It was observed that AWPPH was significantly upregulated in patients with NSCLC, while AWPPH expression level did not increase with the increase of tumor size. In contrast, AWPPH expression levels were significantly higher in patients with distant metastasis than in patients without tumor distant metastasis. AWPPH overexpression promoted TGF-β1 expression in NSCLC cells, while TGF-β1 treatment showed no significant effects on AWPPH expression. AWPPH overexpression promoted NSCLC cell migration and invasion, while TGF-β signaling inhibition reduced this enhancing effect. Therefore, AWPPH may promote the metastasis, but not the growth of NSCLC by upregulating TGF-β1 expression.

LncRNA AWPPH overexpression predicts the recurrence of periodontitis.

Long non-coding RNA (LncRNA) AWPPH is a recently identified oncogenic lncRNA, while its role in other human diseases is still unknown. Blood samples from 80 periodontitis (periodontitis group) patients and 66 healthy controls (control group) who were admitted and treated by Peking University School and Hospital of Stomatology, expression levels of lncRNA AWPPH were detected by RT-PCR. In the present study, we showed that, before treatment, lncRNA AWPPH in plasma was up-regulated in periodontitis patients than in healthy controls. After treatment, expression levels of lncRNA AWPPH reduced significantly. Patients were followed up for 2 years to recorded recurrence. Compared with plasma levels of lncRNA AWPPH on the day of discharge, lncRNA AWPPH expression level increased significantly in patients with recurrence but not in patients without recurrence during follow-up. Based on Youden’s index, patients were divided into high and low lncRNA AWPPH groups according to its expression level on the day of discharge. It was observed that the recurrence rate of periodontitis is significantly higher in high lncRNA AWPPH group than in low lncRNA AWPPH group. LncRNA AWPPH overexpression predicts the recurrence of periodontitis.

Downregulation of lncRNA AWPPH inhibits colon cancer cell proliferation by downregulating GLUT-1.

Long non-coding RNA (lncRNA) associated with poor prognosis of hepatocellular carcinoma (AWPPH) serves pivotal roles in bladder cancer and liver cancer; however, to the best of our knowledge, its functionality in colon cancer has not been characterized. The present study aimed to investigate the involvement of lncRNA AWPPH in colon cancer. Serum levels of lncRNA AWPPH and glucose transporter 1 (GLUT-1) in patients with early stage colon cancer and healthy controls were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and ELISA. Correlation between lncRNA AWPPH and GLUT-1 expression was analyzed by Pearson's correlation coefficient. χ2 test was performed to investigate the associations between serum levels of lncRNA AWPPH and clinical data of patients with colon cancer. lncRNA AWPPH short hairpin RNA and GLUT-1 expression vectors were transfected into colon cancer cells, and the effects on lncRNA AWPPH, GLUT-1 and cell proliferation were detected by RT-qPCR, western blotting and Cell Counting Kit-8 assay. It was observed that serum levels of lncRNA AWPPH and GLUT-1 were significantly higher in patients with colon cancer patients compared with healthy controls. Serum levels of AWPPH and GLUT-1 were significantly positively correlated in patients with colon cancer. Serum levels of lncRNA AWPPH were associated with the tumor size. Furthermore, AWPPH-silencing significantly inhibited GLUT-1 expression and inhibited cancer cell proliferation. GLUT-1 overexpression promoted cancer cell proliferation and attenuated the inhibitory effects of AWPPH-silencing on cancer cell proliferation. However, GLUT-1 overexpression failed to significantly affect the expression of AWPPH. Therefore, it can be concluded that a downregulation of lncRNA AWPPH may inhibit colon cancer cell proliferation by downregulating GLUT-1.

LncRNA AWPPH promotes osteosarcoma progression via activation of Wnt/β-catenin pathway through modulating miR-93-3p/FZD7 axis

Long noncoding RNAs (lncRNAs) have important regulatory roles in osteosarcoma (OS) progression. Recent researches have shown lncRNA AWPPH promotes lung cancer progression and bladder cancer development. Yet, the function of AWPPH in OS is unknown. In this research, results indicated AWPPH levels were increased in OS tissues in contrast to paracancerous controls. Up-regulated AWPPH was associated with advanced stage, tumor size and metastasis. Besides, AWPPH up-regulation indicated a low survival rate in OS patients. Silencing of AWPPH suppressed proliferation, migration and invasion of OS cells. Mechanistically, AWPPH was demonstrated to sponge miR-93-3p and promote FZD7 expression, causing activation of Wnt/β-catenin. Inhibition of miR-93-3p effectively reversed the effects of AWPPH knockdown on OS cells. Collectively, our findings suggested AWPPH may be a prognostic biomarker and potential therapeutic target. AWPPH enhances FZD7-mediated activation of Wnt/β-catenin by sponging miR-93-3p to promote OS progression.

LncRNA AWPPH and miRNA-21 regulates cancer cell proliferation and chemosensitivity in triple-negative breast cancer by interacting with each other.

Long-non-coding RNAs (lncRNA) AWPPH promotes the progression of liver and bladder cancer, indicating its oncogenic role. The current study aimed to explore the involvement of AWPPH in triple-negative breast cancer (TNBC). In the current study, we found that plasma levels of lncRNA AWPPH and microRNA-21 (miRNA-21) were upregulated in patients with TNBC than in healthy controls, and the upregulation of plasma lncRNA AWPPH and miRNA-21 distinguished early-stage patients with TNBC from healthy controls. Plasma levels of lncRNA AWPPH and miRNA-21 were significantly and positively correlated in both patients with TNBC and healthy controls. LncRNA AWPPH and miRNA-21 overexpression led to promoted cancer cells proliferation and improved cancer cell viability under carboplatin treatment, while lncRNA AWPPH small interfering RNA (siRNA) silencing played an opposite role. In addition, miRNA-21 overexpression attenuated the effects of lncRNA AWPPH siRNA silencing on of cancer cell behaviors. LncRNA AWPPH overexpression led to upregulated miRNA-21 in TNBC cells, while miRNA-21 overexpression also led to significantly upregulated lncRNA AWPPH expression. Therefore, lncRNA AWPPH and miRNA-21 may regulate cancer cell proliferation and chemosensitivity in TNBC by interacting with each other.

Long Non-Coding RNA AWPPH Promotes Postoperative Distant Recurrence in Resected Non-Small Cell Lung Cancer by Upregulating Transforming Growth Factor beta 1 (TGF-β1).

BackgroundPostoperative recurrence of cancers is responsible for a large portion of deaths in cancer patients. Our study investigated the involvement of lncRNA AWPPH in recurrence of resected non-small cell lung cancer (NSCLC).Material/MethodsA total of 128 patients were followed up for 3 years. Blood was extracted from each patient on the day of discharge, the day of the diagnosis of recurrence, or at the end of follow-up. Blood from 30 healthy controls was used as a control group. Patient were divided into 3 groups – a non-recurrence group (NR, n=54), a local recurrence group (LR, n=42), and a distant recurrence (DR, n=32) group – according to the follow-up results. Blood AWPPP was detected by qRT-PCR. AWPPH expression vectors were transfected into cells of human NSCLC cell lines. Cell migration and invasion were detected by Transwell migration and invasion assay, respectively. TGF-β1 expression was detected by Western blot analysis.ResultsBlood AWPPH levels were the highest in the DR group, followed by the LR and NR groups. The lowest blood AWPPH levels were observed in the control group. Blood AWPPH levels increased significantly in the DR group but not in the NR and LR groups during follow-up. Blood AWPPH levels were positively correlated with TGF-β1 mRNA levels in the DR group but not in the NR and LR groups during follow-up. AWPPH overexpression promoted cell migration and invasion and upregulated TGF-β1 expression.ConclusionslncRNA AWPPH can promote postoperative distant recurrence in resected NSCLC by upregulating TGF-β1.

LncRNA AWPPH promotes proliferation and inhibits apoptosis of non‑small cell lung cancer cells by activating the Wnt/β‑catenin signaling pathway.

AWPPH is a newly discovered long non‑coding (lnc)RNA that serves an oncogenic role in the development of several types of cancer; however, its involvement in non‑small cell lung cancer (NSCLC) is unknown. Therefore, the aim of the present study was to investigate the function of AWPPH in NSCLC. The results demonstrated that AWPPH expression levels were significantly upregulated in the lung tissues and serum samples of patients with NSCLC compared with in healthy controls. High expression levels of AWPPH effectively distinguished NSCLC patients from healthy controls. In addition, patients with high expression levels of AWPPH had significantly shorter survival time. AWPPH overexpression in NSCLC cells promoted proliferation and inhibited apoptosis, and activated the Wnt/β‑catenin signaling pathway, which is a classic signaling pathway involved in the development and progression of different types of cancers. Treatment with a Wnt/β‑catenin signaling pathway activator produced no significant effect on AWPPH expression. Therefore, it was concluded that lcRNA AWPPH could promote the growth of NSCLCs by activating the Wnt/β‑catenin signaling pathway.