scholarly journals Tobacco carcinogen-induced mouse lung adenocarcinoma cell lines as tools to identify novel lung cancer genes

2018 ◽  
Author(s):  
Νικόλαος Κανελλάκης
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Mouse Lung ◽  
Cancer Genes ◽  
Adenocarcinoma Cell ◽  
Tobacco Carcinogen

Η νόσος του καρκίνου αποτελεί ένα σημαντικό και βαρύ κοινωνικό-οικονομικό φορτίο τόσο για τις οικονομικά αναπτυγμένες όσο και για τις οικονομικά αναπτυσσόμενες κοινωνίες. Η συχνότητα της διάγνωσης καρκινικών περιστατικών δείχνει να αυξάνεται με την πάροδο του χρόνου λόγω της γήρανσης του πληθυσμού και της αδυναμίας περιορισμού της χρήσης παραγόντων οι οποίοι έχουν συσχετιστεί με τον κίνδυνο εμφάνισης καρκίνου, όπως το κάπνισμα. Ο καρκίνος του πνεύμονα αποτελεί την κύρια αιτία θανάτου από καρκίνο παγκοσμίως. Οι κακοήθειες οι οποίες επάγονται από καρκινογόνα, συμπεριλαμβανομένου του πνευμονικού αδενοκαρκινώματος των καπνιστών, περιέχουν χιλιάδες μεταλλάξεις στο γονιδίωμά τους. Τις τελευταίες δεκαετίες έχουν ανακαλυφθεί και μελετηθεί πολλά νέα ογκογονίδια συσχετιζόμενα με το αδενοκαρκίνωμα πνεύμονα με αποτέλεσμα να εισαχθούν στην κλινική πράξη νέοι αντικαρκινικοί παράγοντες οι οποίοι άλλαξαν την πρόγνωση των ασθενών και βελτίωσαν την ποιότητα της ζωής τους. Ωστόσο, λόγω περιορισμών σχεδόν στα μισά περιστατικά τα ογκογονίδια τα οποία ευθύνονται για την ανάπτυξη των νεοπλασμάτων δεν είναι δυνατό να εντοπιστούν και έτσι παραμένουν άγνωστα. Παρά την ύπαρξη περίτεχνων γενετικών μοντέλων ποντικών του καρκίνου του πνεύμονα, αδυνατούν να προσομοιώσουν την ανθρώπινη νόσο με ακρίβεια και πιστότητα. Η ανάπτυξη ενός αξιόπιστου μοντέλου ποντικών το οποίο θα μπορούσε να χρησιμοποιηθεί για την εντοπισμό των ογκογονιδίων και μεταλλάξεων του καρκίνου πνεύμονα παραμένει μια μη ικανοποιημένη και ιδιαίτερα σημαντική ερευνητική ανάγκη. Καταφέραμε να αναπτύξουμε μια μεθοδολογία για τη δημιουργία κυτταρικών σειρών αδενοκαρκινώματος πνεύμονα ποντικού από διάφορα στελέχη μετά από επαναλαμβανόμενη έκθεση στις καρκινογόνες ουσίες του καπνού: ουρεθάνη και διαιθυλο νιτροζαμίνη. Οι κυτταρικές σειρές οι οποίες προέκυψαν (n = 7) ήταν αθάνατες και φαινοτυπικά σταθερές in vitro, ογκογόνες, μεταστατικές και θανατηφόρες in vivo. Οι επαγόμενες από χημικά καρκινογόνα του καπνού κυτταρικές σειρές παρουσίασαν αξιοσημείωτη ομοιότητα με το ανθρώπινο αδενοκαρκίνωμα πνεύμονα, καθώς περιείχαν μεταλλάξεις στα γονίδια Kras και Trp53 και παρουσίασαν χαρακτηριστικές ιδιότητες των καρκινικών βλαστοκυττάρων. Ανακαλύψαμε ότι όλες οι κυτταρικές σειρές υπερέκφραζαν το γονίδιο Proliferin, ένα ορθολογo στον ποντικό για την ανθρώπινη προλακτίνη. Η λειτουργική μελέτη του γονιδίου έδειξε πως δρα ως υποκινητής για την αναπτυξη πνευμονικών όγκων. Είναι ενδιαφέρον το γεγονός πως η προλακτίνη βρέθηκε υπερεκφρασμένη και συσχετίστηκε με κακή πρόγνωση στο ανθρώπινο αδενοκαρκίνωμα πνεύμονα. Συμπερασματικά τα κύτταρα αδενοκαρκινώματος πνεύμονα ποντικού τα οποία δημιουργήσαμε με τη χρήση καρκινογόνων του καπνού μοιάζουν με την ανθρώπινη νόσο του αδενοκαρκινώματος πνεύμονα. Ως εκ τούτου μπορούν να χρησιμοποιηθούν ως ένα πολύτιμο εργαλείο για την ανακάλυψη και τη λειτουργική διερεύνηση νέων ογκογονιδίων του αδενοκαρκινώματος του πνεύμονα, των μεταλλάξεων που οδηγούν στην ανάπτυξή του και των βιολογικών μονοπατιών και μηχανισμών που προάγουν την πνευμονική καρκινογένεση.ΛΕΞΕΙΣ ΚΛΕΙΔΙΑπνεύμονας; αδενοκαρκίνωμα; καπνός; καρκινογόνο; κάπνισμα; KRAS; TRP53

scholarly journals LSC - 2017 - Mouse lung adenocarcinoma cell lines as tools to identify novel lung cancer genes

2017 ◽  
Author(s):  
Nikolaos Kanellakis ◽  
Anastasios Giannou ◽  
Theodora Agalioti ◽  
Rahul Prashanth Ravindran ◽  
Dimitra Zazara ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Mouse Lung ◽  
Cancer Genes ◽  
Adenocarcinoma Cell

scholarly journals Lung adenocarcinoma cell-derived exosomal miR-328 promote osteoclastogenesis by targeting Nrp2

2021 ◽  
Author(s):  
Cheng Cheng Zhang ◽  
Jingru Qin ◽  
Lu Yang ◽  
Zhiyao Zhu ◽  
Xinle Qian ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Bone Metastasis ◽  
Bone Resorption ◽  
Lung Adenocarcinoma ◽  
Adenocarcinoma Cell ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Bone metastasis of lung cancer and detailed mechanisms are still elusive, and the roles of exosomes derived from lung adenocarcinoma cells in this process have attracted much attention. In this study, we found that lung adenocarcinoma cell-derived exosomes (LCC-Exos) promoted osteogenesis and bone resorption in vitro. Furthermore, LCC-Exos target bone in vivo and promoted bone resorption in vivo. Mechanistically, LCC-Exosomal miR-328 promoted bone resorption by targeting Nrp2 and LCC-ExosmiR-328 Inhibitors inhibited bone resorption in vivo. Thus, LCC-Exosomal miR-328 promote osteoclastogenesis by targeting Nrp2 and LCC-ExosmiR-328 Inhibitors may serve as a potential nanomedicine for the treatment of bone metastasis.

scholarly journals UBR-Box containing protein, UBR5, is over-expressed in human lung adenocarcinoma and is a potential therapeutic target

2020 ◽  
Author(s):  
Kumar Saurabh ◽  
Parag P Shah ◽  
Mark Doll ◽  
Leah J Siskind ◽  
Levi J. Beverly
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Viability ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Human Lung ◽  
Human Patient ◽  
Adenocarcinoma Cell ◽  
Ubiquitination Pathway

Abstract Background: N-end rule ubiquitination pathway is known to be disrupted in many diseases, including cancer. UBR5, an E3 ubiquitin ligase, is mutated and/or overexpressed in human lung cancer cells suggesting its pathological role in cancer. Methods: We determined expression of UBR5 protein in multiple lung cancer cell lines and human patient samples. Using immunoprecipitation followed by mass spectrometry we determined the UBR5 interacting proteins. The impact of loss of UBR5 for lung adenocarcinoma cell lines was analyzed using cell viability, clonogenic assays and in vivo xenograft models in nude mice. Additional Western blot analysis was performed to assess the loss of UBR5 on downstream signaling. Statistical analysis was done by one-way ANOVA for in vitro studies and Wilcoxon paired t-test for tumor volumes in vivo. Results: We show variability of UBR5 expression levels in lung adenocarcinoma cell lines and in primary human patient samples. To gain better insight into the role that UBR5 may play in lung cancer progression we performed unbiased interactome analyses for UBR5. Data indicate that UBR5 has a wide range of interacting protein partners that are known to be involved in critical cellular processes such as DNA damage, proliferation and cell cycle regulation. We have demonstrated that shRNA-mediated loss of UBR5 decreases cell viability and clonogenic potential of lung adenocarcinoma cell lines. In addition, we found decreased levels of activated AKT signaling after the loss of UBR5 in lung adenocarcinoma cell lines using multiple means of UBR5 knockdown/knockout. Furthermore, we demonstrated that loss of UBR5 in lung adenocarcinoma cells results in significant reduction of tumor volume in nude mice. Conclusions: These findings demonstrate that deregulation of the N-end rule ubiquitination pathway plays a crucial role in the etiology of some human cancers, and blocking this pathway via UBR5-specific inhibitors, may represent a unique therapeutic target for human cancers.

scholarly journals UBR-Box containing protein, UBR5, is over-expressed in human lung adenocarcinoma and is a potential therapeutic target

2020 ◽  
Author(s):  
Kumar Saurabh ◽  
Parag P. Shah ◽  
Mark A. Doll ◽  
Leah J. Siskind ◽  
Levi J. Beverly
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Viability ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Human Lung ◽  
Human Patient ◽  
Adenocarcinoma Cell ◽  
Ubiquitination Pathway

AbstractBackgroundN-end rule ubiquitination pathway is known to be disrupted in many diseases, including cancer. UBR5, an E3 ubiquitin ligase, is mutated and/or overexpressed in human lung cancer cells suggesting its pathological role in cancer.MethodsWe determined expression of UBR5 protein in multiple lung cancer cell lines and human patient samples. Using immunoprecipitation followed by mass spectrometry we determined the UBR5 interacting proteins. The impact of loss of UBR5 for lung adenocarcinoma cell lines was analyzed using cell viability, clonogenic assays and in vivo xenograft models in nude mice. Additional Western blot analysis was performed to assess the loss of UBR5 on downstream signaling. Statistical analysis was done by one-way ANOVA for in vitro studies and Wilcoxon paired t-test for tumor volumes in vivo.ResultsWe show variability of UBR5 expression levels in lung adenocarcinoma cell lines and in primary human patient samples. To gain better insight into the role that UBR5 may play in lung cancer progression we performed unbiased interactome analyses for UBR5. Data indicate that UBR5 has a wide range of interacting protein partners that are known to be involved in critical cellular processes such as DNA damage, proliferation and cell cycle regulation. We have demonstrated that shRNA-mediated loss of UBR5 decreases cell viability and clonogenic potential of lung adenocarcinoma cell lines. In addition, we found decreased levels of activated AKT signaling after the loss of UBR5 in lung adenocarcinoma cell lines using multiple means of UBR5 knockdown/knockout. Furthermore, we demonstrated that loss of UBR5 in lung adenocarcinoma cells results in significant reduction of tumor volume in nude mice.ConclusionsThese findings demonstrate that deregulation of the N-end rule ubiquitination pathway plays a crucial role in the etiology of some human cancers, and blocking this pathway via UBR5-specific inhibitors, may represent a unique therapeutic target for human cancers.

scholarly journals UBR-Box containing protein, UBR5, is over-expressed in human lung adenocarcinoma and is a potential therapeutic target

2020 ◽  
Author(s):  
Kumar Saurabh ◽  
Parag P Shah ◽  
Mark Doll ◽  
Leah J Siskind ◽  
Levi J. Beverly
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Viability ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Human Lung ◽  
Human Patient ◽  
Adenocarcinoma Cell ◽  
Ubiquitination Pathway

Abstract Background: N-end rule ubiquitination pathway is known to be disrupted in many diseases, including cancer. UBR5, an E3 ubiquitin ligase, is mutated and/or overexpressed in human lung cancer cells suggesting its pathological role in cancer. Methods: We determined expression of UBR5 protein in multiple lung cancer cell lines and human patient samples. Using immunoprecipitation followed by mass spectrometry we determined the UBR5 interacting proteins. The impact of loss of UBR5 for lung adenocarcinoma cell lines was analyzed using cell viability, clonogenic assays and in vivo xenograft models in nude mice. Additional Western blot analysis was performed to assess the loss of UBR5 on downstream signaling. Statistical analysis was done by one-way ANOVA for in vitro studies and Wilcoxon paired t-test for tumor volumes in vivo. Results: We show variability of UBR5 expression levels in lung adenocarcinoma cell lines and in primary human patient samples. To gain better insight into the role that UBR5 may play in lung cancer progression we performed unbiased interactome analyses for UBR5. Data indicate that UBR5 has a wide range of interacting protein partners that are known to be involved in critical cellular processes such as DNA damage, proliferation and cell cycle regulation. We have demonstrated that shRNA-mediated loss of UBR5 decreases cell viability and clonogenic potential of lung adenocarcinoma cell lines. In addition, we found decreased levels of activated AKT signaling after the loss of UBR5 in lung adenocarcinoma cell lines using multiple means of UBR5 knockdown/knockout. Furthermore, we demonstrated that loss of UBR5 in lung adenocarcinoma cells results in significant reduction of tumor volume in nude mice. Conclusions: These findings demonstrate that deregulation of the N-end rule ubiquitination pathway plays a crucial role in the etiology of some human cancers, and blocking this pathway via UBR5-specific inhibitors, may represent a unique therapeutic target for human cancers.

scholarly journals RETRACTED ARTICLE: Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma

2016 ◽  
Vol 7 (9) ◽  
pp. e2388-e2388 ◽  
Author(s):  
Shuang Wei ◽  
Zun-yi Zhang ◽  
Sheng-ling Fu ◽  
Jun-gang Xie ◽  
Xian-sheng Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Kinase Inhibitor ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Adenocarcinoma Cell ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Abstract Our previous study revealed that Ku80 was overexpressed in lung cancer tissues and hsa-miR-623 regulated the Ku80 expression; however, the detailed function of hsa-miR-623 in lung cancer was unclear. We identified that hsa-miR-623 bound to the 3'-UTR of Ku80 mRNA, thus significantly decreasing Ku80 expression in lung adenocarcinoma cells. Hsa-miR-623 was downregulated in lung adenocarcinoma tissues compared with corresponding non-tumorous tissues, and its expression was inversely correlated with Ku80 upregulation. Downregulation of hsa-miR-623 was associated with poor clinical outcomes of lung adenocarcinoma patients. Hsa-miR-623 suppressed lung adenocarcinoma cell proliferation, clonogenicity, migration and invasion in vitro. Hsa-miR-623 inhibited xenografts growth and metastasis of lung adenocarcinoma in vivo. Ku80 knockdown in lung adenocarcinoma cells suppressed tumor properties in vitro and in vivo similar to hsa-miR-623 overexpression. Further, hsa-miR-623 overexpression decreased matrix metalloproteinase-2 (MMP-2) and MMP-9 expression levels, with decreased ERK/JNK phosphorylation. Inhibition of hsa-miR-623 or overexpression of Ku80 promoted lung adenocarcinoma cell invasion, activated ERK/JNK phosphorylation and increased MMP-2/9 expressions, which could be reversed by ERK kinase inhibitor or JNK kinase inhibitor. In summary, our results showed that hsa-miR-623 was downregulated in lung adenocarcinoma and suppressed the invasion and metastasis targeting Ku80 through ERK/JNK inactivation mediated downregulation of MMP-2/9. These findings reveal that hsa-miR-623 may serve as an important therapeutic target in lung cancer therapy.

Tobacco chemical-induced mouse lung adenocarcinoma cell lines pin the prolactin orthologue proliferin as a lung tumour promoter

2019 ◽  
Vol 40 (11) ◽  
pp. 1352-1362 ◽  
Author(s):  
Nikolaos I Kanellakis ◽  
Anastasios D Giannou ◽  
Mario A A Pepe ◽  
Theodora Agalioti ◽  
Dimitra E Zazara ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Mouse Models ◽  
Cell Lines ◽  
Point Mutations ◽  
Mouse Lung ◽  
Mouse Strains ◽  
Lung Tumour ◽  
Tobacco Carcinogens

Abstract Lung adenocarcinoma (LADC) is the leading cause of cancer death worldwide. Nevertheless, syngeneic mouse models of the disease are sparse, and cell lines suitable for transplantable and immunocompetent mouse models of LADC remain unmet needs. We established multiple mouse LADC cell lines by repeatedly exposing two mouse strains (FVB, Balb/c) to the tobacco carcinogens urethane or diethylnitrosamine and by culturing out the resulting lung tumours for prolonged periods of time. Characterization of the resulting cell lines (n = 7) showed that they were immortal and phenotypically stable in vitro, and oncogenic, metastatic and lethal in vivo. The primary tumours that gave rise to the cell lines, as well as secondary tumours generated by transplantation of the cell lines, displayed typical LADC features, such as glandular architecture and mucin and thyroid transcription factor 1 expression. Moreover, these cells exhibited marked molecular similarity with human smokers’ LADC, including carcinogen-specific Kras point mutations (KrasQ61R in urethane- and KrasQ61H in diethylnitrosamine-triggered cell lines) and Trp53 deletions and displayed stemness features. Interestingly, all cell lines overexpressed proliferin, a murine prolactin orthologue, which functioned as a lung tumour promoter. Furthermore, prolactin was overexpressed and portended poor prognosis in human LADC. In conclusion, we report the first LADC cell lines derived from mice exposed to tobacco carcinogens. These cells closely resemble human LADC and provide a valuable tool for the functional investigation of the pathobiology of the disease.

scholarly journals UBR-Box Containing Protein, UBR5, is Over-Expressed in Human Lung Adenocarcinoma and is a Potential Therapeutic Target

2020 ◽  
Author(s):  
Kumar Saurabh ◽  
Parag P Shah ◽  
Mark Doll ◽  
Leah J Siskind ◽  
Levi J. Beverly
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Nude Mice ◽  
Therapeutic Target ◽  
Human Lung ◽  
Human Patient ◽  
Adenocarcinoma Cell ◽  
Ubiquitination Pathway

Abstract Background:N-end rule ubiquitination pathway is known to be disrupted in many diseases, including cancer. UBR5, an E3 ubiquitin ligase, is mutated and/or overexpressed in human lung cancer cells suggesting its pathological role in cancer. Methods: We determined expression of UBR5 protein in multiple lung cancer cell lines and human patient samples.Using immunoprecipitation followed by mass spectrometry we determined the UBR5 interacting proteins. The impact of loss of UBR5 for lung adenocarcinoma cell lines was analyzed using cell viability, clonogenic assays and in vivo xenograft models in nude mice. Additional Western blot analysis was performed to assess the loss of UBR5 on downstream signaling. Statistical analysis was done by one-way ANOVA for in vitro studies and Wilcoxon paired t-test for tumor volumes in vivo.Results:We show variability of UBR5 expression levels in lung adenocarcinoma cell lines and in primary human patient samples.To gain better insight into the role that UBR5 may play in lung cancer progression we performed unbiased interactome analyses for UBR5. Dataindicate that UBR5 has a wide range of interacting protein partners that are known to be involved in critical cellular processes such as DNA damage, proliferation and cell cycle regulation. We have demonstrated thatshRNA-mediated lossof UBR5 decreases cell viabilityand clonogenic potential of lung adenocarcinoma cell lines.In addition, we founddecreased levels of activatedAKT signaling after the loss of UBR5 in lung adenocarcinoma cell lines using multiple means of UBR5 knockdown/knockout. Furthermore, we demonstrated that loss of UBR5 in lung adenocarcinoma cells results in significant reduction of tumor volume in nude mice. Conclusions:These findings demonstrate that deregulation of the N-end rule ubiquitination pathway plays a crucial role in the etiology of some human cancers, and blocking this pathway via UBR5-specific inhibitors, may represent a unique therapeutic target for human cancers.

scholarly journals Urinary detection of lung cancer in mice via noninvasive pulmonary protease profiling

2020 ◽  
Vol 12 (537) ◽  
pp. eaaw0262 ◽  
Author(s):  
Jesse D. Kirkpatrick ◽  
Andrew D. Warren ◽  
Ava P. Soleimany ◽  
Peter M. K. Westcott ◽  
Justin C. Voog ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Genetically Engineered ◽  
Mouse Lung ◽  
National Guidelines ◽  
Stage Disease ◽  
Risk Patients ◽  
Localized Disease

Lung cancer is the leading cause of cancer-related death, and patients most commonly present with incurable advanced-stage disease. U.S. national guidelines recommend screening for high-risk patients with low-dose computed tomography, but this approach has limitations including high false-positive rates. Activity-based nanosensors can detect dysregulated proteases in vivo and release a reporter to provide a urinary readout of disease activity. Here, we demonstrate the translational potential of activity-based nanosensors for lung cancer by coupling nanosensor multiplexing with intrapulmonary delivery and machine learning to detect localized disease in two immunocompetent genetically engineered mouse models. The design of our multiplexed panel of sensors was informed by comparative transcriptomic analysis of human and mouse lung adenocarcinoma datasets and in vitro cleavage assays with recombinant candidate proteases. Intrapulmonary administration of the nanosensors to a Kras- and Trp53-mutant lung adenocarcinoma mouse model confirmed the role of metalloproteases in lung cancer and enabled accurate detection of localized disease, with 100% specificity and 81% sensitivity. Furthermore, this approach generalized to an alternative autochthonous model of lung adenocarcinoma, where it detected cancer with 100% specificity and 95% sensitivity and was not confounded by lipopolysaccharide-driven lung inflammation. These results encourage the clinical development of activity-based nanosensors for the detection of lung cancer.

LncRNA SNHG4 promotes the proliferation, migration, invasiveness, and epithelial–mesenchymal transition of lung cancer cells by regulating miR-98-5p

2019 ◽  
Vol 97 (6) ◽  
pp. 767-776 ◽  
Author(s):  
Yufu Tang ◽  
Lijian Wu ◽  
Mingjing Zhao ◽  
Guangdan Zhao ◽  
Shitao Mao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Lung Cancer Cells ◽  
Mesenchymal Transition ◽  
Gene 4

Long noncoding RNA small nucleolar RNA host gene 4 (SNHG4) is usually up-regulated in cancer and regulates the malignant behavior of cancer cells. However, its role in lung cancer remains elusive. In this study, we silenced the expression of SNHG4 in NCI-H1437 and SK-MES-1, two representative non-small-cell lung cancer cell lines, by transfecting them with siRNA (small interfering RNA) that specifically targets SNHG4. We observed significantly inhibited cell proliferation in vitro and reduced tumor growth in vivo after SNHG4 silencing. SNHG4 knockdown also led to cell cycle arrest at the G1 phase, accompanied with down-regulation of cyclin-dependent kinases CDK4 and CDK6. The migration and invasiveness of these two cell lines were remarkably inhibited after SNHG4 silencing. Moreover, our study revealed that the epithelial–mesenchymal transition (EMT) of lung cancer cells was suppressed by SNHG4 silencing, as evidenced by up-regulated E-cadherin and down-regulated SALL4, Twist, and vimentin. In addition, we found that SNHG4 silencing induced up-regulation of miR-98-5p. MiR-98-5p inhibition abrogated the effect of SNHG4 silencing on proliferation and invasion of lung cancer cells. In conclusion, our findings demonstrate that SNHG4 is required by lung cancer cells to maintain malignant phenotype. SNHG4 probably exerts its pro-survival and pro-metastatic effects by sponging anti-tumor miR-98-5p.

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