Juan Li1,2, Yifan Lian1,2, Changsheng Yan3, Zeling Cai4, Jie Ding2, Zhonghua Ma2, Peng Peng2, Keming Wang1,2. 1. The Second Clinical Medical College of Nanjing Medical University, Nanjing, Jiangsu, China. 2. Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. 3. Department of Obstetrics and Gynecology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China. 4. Department of General Surgery, Second Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Abstract
OBJECTIVES: Despite improvements in diagnosis and treatment, colorectal cancer (CRC) remains the third most common malignancy, and fourth-leading cause of cancer-related death worldwide, and has a particularly high incidence in Western countries. Recent studies have suggested that long non-coding RNAs (lncRNAs) compose a novel class of regulators of cancer biological processes, such as proliferation, apoptosis and metastasis. Here, we report that lncRNA FOXP4-AS1 acts as a functional oncogene in CRC pathogenesis. Moreover, we have attempted to investigate the effects of FOXP4-AS1 on tumour progression, both in vitro and in vivo. MATERIALS AND METHODS: In this study, bioinformatic analyses and qPCR were performed to investigate FOXP4-AS1 expression in CRC tissue samples and CRC cell lines. We inhibited FOXP4-AS1 expression via FOXP4-AS1-specific siRNA transfection. Cell proliferation was assessed using cell viability and colony formation assays, as well as by flow cytometry and ethynyl deoxyuridine (Edu) analyses. Apoptosis was assessed using flow cytometry. Animal tumour xenografts were generated, and immunohistochemistry (IHC) was performed to evaluate effects of FOXP4-AS1 on CRC tumour growth in vivo. RESULTS: We found that FOXP4-AS1 was up-regulated in CRC tissues and cell lines and that its overexpression positively correlated with advanced pathological stages and larger tumour size. Additionally, we found that FOXP4-AS1 knockdown inhibited cell proliferation and induced apoptosis. Furthermore, FOXP4-AS1 knockdown induced marked increase in number of cells in G0/G1 phase and reduction in number of cells in S phase, in DLD-1, HT-29 and HCT116 cell lines. Consistent with these findings, FOXP4-AS1 silencing inhibited tumour growth in vivo. CONCLUSION: These findings suggest that FOXP4-AS1 plays a crucial role in CRC progression and may be a new biomarker in patients with CRC.
OBJECTIVES: Despite improvements in diagnosis and treatment, colorectal cancer (CRC) remains the third most common malignancy, and fourth-leading cause of cancer-related death worldwide, and has a particularly high incidence in Western countries. Recent studies have suggested that long non-coding RNAs (lncRNAs) compose a novel class of regulators of cancer biological processes, such as proliferation, apoptosis and metastasis. Here, we report that lncRNA FOXP4-AS1 acts as a functional oncogene in CRC pathogenesis. Moreover, we have attempted to investigate the effects of FOXP4-AS1 on tumour progression, both in vitro and in vivo. MATERIALS AND METHODS: In this study, bioinformatic analyses and qPCR were performed to investigate FOXP4-AS1 expression in CRC tissue samples and CRC cell lines. We inhibited FOXP4-AS1 expression via FOXP4-AS1-specific siRNA transfection. Cell proliferation was assessed using cell viability and colony formation assays, as well as by flow cytometry and ethynyl deoxyuridine (Edu) analyses. Apoptosis was assessed using flow cytometry. Animal tumour xenografts were generated, and immunohistochemistry (IHC) was performed to evaluate effects of FOXP4-AS1 on CRC tumour growth in vivo. RESULTS: We found that FOXP4-AS1 was up-regulated in CRC tissues and cell lines and that its overexpression positively correlated with advanced pathological stages and larger tumour size. Additionally, we found that FOXP4-AS1 knockdown inhibited cell proliferation and induced apoptosis. Furthermore, FOXP4-AS1 knockdown induced marked increase in number of cells in G0/G1 phase and reduction in number of cells in S phase, in DLD-1, HT-29 and HCT116 cell lines. Consistent with these findings, FOXP4-AS1 silencing inhibited tumour growth in vivo. CONCLUSION: These findings suggest that FOXP4-AS1 plays a crucial role in CRC progression and may be a new biomarker in patients with CRC.
Authors: Sarah Djebali; Carrie A Davis; Angelika Merkel; Alex Dobin; Timo Lassmann; Ali Mortazavi; Andrea Tanzer; Julien Lagarde; Wei Lin; Felix Schlesinger; Chenghai Xue; Georgi K Marinov; Jainab Khatun; Brian A Williams; Chris Zaleski; Joel Rozowsky; Maik Röder; Felix Kokocinski; Rehab F Abdelhamid; Tyler Alioto; Igor Antoshechkin; Michael T Baer; Nadav S Bar; Philippe Batut; Kimberly Bell; Ian Bell; Sudipto Chakrabortty; Xian Chen; Jacqueline Chrast; Joao Curado; Thomas Derrien; Jorg Drenkow; Erica Dumais; Jacqueline Dumais; Radha Duttagupta; Emilie Falconnet; Meagan Fastuca; Kata Fejes-Toth; Pedro Ferreira; Sylvain Foissac; Melissa J Fullwood; Hui Gao; David Gonzalez; Assaf Gordon; Harsha Gunawardena; Cedric Howald; Sonali Jha; Rory Johnson; Philipp Kapranov; Brandon King; Colin Kingswood; Oscar J Luo; Eddie Park; Kimberly Persaud; Jonathan B Preall; Paolo Ribeca; Brian Risk; Daniel Robyr; Michael Sammeth; Lorian Schaffer; Lei-Hoon See; Atif Shahab; Jorgen Skancke; Ana Maria Suzuki; Hazuki Takahashi; Hagen Tilgner; Diane Trout; Nathalie Walters; Huaien Wang; John Wrobel; Yanbao Yu; Xiaoan Ruan; Yoshihide Hayashizaki; Jennifer Harrow; Mark Gerstein; Tim Hubbard; Alexandre Reymond; Stylianos E Antonarakis; Gregory Hannon; Morgan C Giddings; Yijun Ruan; Barbara Wold; Piero Carninci; Roderic Guigó; Thomas R Gingeras Journal: Nature Date: 2012-09-06 Impact factor: 49.962
Authors: Zheng Li; Xingye Li; Chong Chen; Shugang Li; Jianxiong Shen; Gary Tse; Matthew T V Chan; William K K Wu Journal: Cell Prolif Date: 2018-07-24 Impact factor: 6.831