Cancer Research and Treatment

Original Articles

Gastrointestinal cancer

The Oncogenic Role of TNFRSF12A in Colorectal Cancer and Pan-Cancer Bioinformatics Analysis: Chuyue Wang, Yingying Zhao, You Chen, Ying Shi, Zhiying Yang, Weili Wu, Rui Ma, Bo Wang, Yifeng Sun, Ping Yuan; Cancer Res Treat. 2025;57(1):212-228. Published online August 9, 2024; DOI: https://doi.org/10.4143/crt.2024.408

Abstract PDF Supplementary Material PubReader ePub: Purpose
Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms.
Materials and Methods
Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A.
Results
TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer.
Conclusion
TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

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Sarcoma

Enrichment of Wee1/CDC2 and NF-κB Signaling Pathway Constituents Mutually Contributes to CDDP Resistance in Human Osteosarcoma: Zhengbo Hu, Lugen Li, Wenxing Lan, Xiao Wei, Xiangyuan Wen, Penghuan Wu, Xianliao Zhang, Xinhua Xi, Yufa Li, Liqi Wu, Wenhu Li, Xiaohong Liao; Cancer Res Treat. 2022;54(1):277-293. Published online May 11, 2021; DOI: https://doi.org/10.4143/crt.2021.320

Abstract PDF PubReader ePub

Purpose
Osteosarcoma (OS) universally exhibits heterogeneity and cisplatin (CDDP) resistance. Although the Wee1/CDC2 and nuclear factor кB (NF-κB) pathways were reported to show abnormal activation in some tumor cells with CDDP resistance, whether there is any concrete connection is currently unclear. We explored it in human OS cells.
Materials and Methods
Multiple OS cell lines were exposed to a Wee1 inhibitor (AZD1775) and CDDP to assess the half-maximal inhibitory concentration values. Western blot, coimmunoprecipitation, confocal immunofluorescence, cell cycle, and Cell Counting Kit-8assays were performed to explore the connection between the Wee1/CDC2 and NF-κB pathways and their subsequent physiological contribution to CDDP resistance. Finally, CDDP-resistant PDX-OS xenograft models were established to confirm that AZD1775 restores the antitumor effects of CDDP.
Results
A sensitivity hierarchy of OS cells to CDDP and AZD1775 exists. In the highly CDDP-tolerant cell lines, Wee1 and RelA were physically crosslinked, which resulted in increased abundance of phosphorylated CDC2 (Y15) and RelA (S536) and consequent modulation of cell cycle progression, survival, and proliferation. Wee1 inhibition restored the effects of CDDP on these processes in CDDP-resistant OS cells. In addition, animal experiments with CDDP-resistant PDX-OS cells showed that AZD1775 combined with CDDP not only restored CDDP efficacy but also amplified AZD1775 in inhibiting tumor growth and prolonged the median survival of the mice.
Conclusion
Simultaneous enrichment of molecules in the Wee1/CDC2 and NF-κB pathways and their consequent coactivation is a new molecular mechanism of CDDP resistance in OS cells. OS with this molecular signature may respond well to Wee1 inhibition as an alternative treatment strategy.

Citations

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Wee1 inhibitor PD0166285 sensitized TP53 mutant lung squamous cell carcinoma to cisplatin via STAT1
Qi Li, Wenjie Yang, Qingyi Zhang, Daoming Zhang, Jun Deng, Binxin Chen, Ping Li, Huanqi Zhang, Yiming Jiang, Yangling Li, Bo Zhang, Nengming Lin
Cancer Cell International.2024;[Epub] CrossRef
BRK confers tamoxifen-resistance in breast cancer via regulation of tyrosine phosphorylation of CDK1
Aditya Mandapati, Zhibin Ning, Akanksha Baharani, Kiven Erique Lukong
Cellular Signalling.2023; 108: 110723. CrossRef
Inhibiting WEE1 Augments the Antitumor Efficacy of Cisplatin in Urothelial Carcinoma by Enhancing the DNA Damage Process
Yu-Li Su, Ling-Yi Xiao, Shih-Yu Huang, Chia-Che Wu, Li-Chung Chang, Yi-Hua Chen, Hao-Lun Luo, Chun-Chieh Huang, Ting-Ting Liu, Jei-Ming Peng
Cells.2023; 12(11): 1471. CrossRef
Network pharmacology-based research on the effect of angelicin on osteosarcoma and the underlying mechanism
Yafang Zhang, Junqiang Wei, Lingwei Kong, Mingze Song, Yange Zhang, Xiangyu Xiao, Haiying Cao, Zhehong Li, Ning Yang, Yu Jin
Aging.2023;[Epub] CrossRef
Identification of Cell Subpopulations and Interactive Signaling Pathways From a Single-Cell RNA Sequencing Dataset in Osteosarcoma: A Comprehensive Bioinformatics Analysis
Rong Wu, Xiaojie Dou, Haidong Li, Zhenguo Sun, Heng Li, Yuxin Shen, Wei Weng, Jikang Min
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MicroRNAs and osteosarcoma: Potential targets for inhibiting metastasis and increasing chemosensitivity
Negin Soghli, Gordon A. Ferns, Fatemeh Sadeghsoltani, Durdi Qujeq, Tooba Yousefi, Mostafa Vaghari-Tabari
Biochemical Pharmacology.2022; 201: 115094. CrossRef
Inhibiting WEE1 and IKK-RELA Crosstalk Overcomes TNFα Resistance in Head and Neck Cancers
Zhengbo Hu, Ramya Viswanathan, Hui Cheng, Jianghong Chen, Xinping Yang, Angel Huynh, Paul Clavijo, Yi An, Yvette Robbins, Christopher Silvin, Clint Allen, Pinar Ormanoglu, Scott Martin, Shaleeka Cornelius, Anthony Saleh, Zhong Chen, Carter Van Waes, Ethan
Molecular Cancer Research.2022; 20(6): 867. CrossRef
Epithelial to Mesenchymal Transition Relevant Subtypes with Distinct Prognosis and Responses to Chemo- or Immunotherapies in Osteosarcoma
Yang Zhou, Gai Li, Hu Li, Fuchong Lai, Pingguo Duan, Ming Cheng, Fu Wang
Journal of Immunology Research.2022; 2022: 1. CrossRef
Proteasome Inhibitors and Their Potential Applicability in Osteosarcoma Treatment
Cassidy M. Van Stiphout, Anita K. Luu, Alicia M. Viloria-Petit
Cancers.2022; 14(19): 4544. CrossRef

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Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL: Chunhui Cui, Duanyang Zhai, Lianxu Cai, Qiaobin Duan, Lang Xie, Jinlong Yu; Cancer Res Treat. 2018;50(3):992-1008. Published online October 30, 2017; DOI: https://doi.org/10.4143/crt.2017.226

Abstract PDF PubReader ePub

Purpose
Studies have found that long noncoding RNA HEIH (lncRNA-HEIH) is upregulated and facilitates hepatocellular carcinoma tumor growth. However, its clinical significances, roles, and action mechanism in colorectal cancer (CRC) remains unidentified.
Materials and Methods
lncRNA-HEIH expression in CRC tissues and cell lines was measured by quantitative real-time polymerase chain reaction. Cell CountingKit-8, ethynyl deoxyuridine incorporation assay, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and nude mice xenografts assays were performed to investigate the roles of lncRNA-HEIH. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays were performed to investigate the action mechanisms of lncRNA-HEIH.
Results
In this study, we found that lncRNA-HEIH is significantly increased in CRC tissues and cell lines. lncRNA-HEIH expression is positively associated with tumor size, invasion depth, and poor prognosis of CRC patients. Enhanced expression of lncRNA-HEIH promotes CRC cell proliferation and decreases apoptosis in vitro, and promotes CRC tumor growth in vivo. Whereas knockdown of lncRNA-HEIH inhibits CRC cell proliferation and induces apoptosis in vitro, and suppresses CRC tumor growth in vivo. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor κB (NF-κB), increases the binding of NF-κB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL. Moreover, Bcl-xL expression is positively associatedwith lncRNA-HEIH in CRC tissues. Blocking the interaction between lncRNA-HEIH and miR-939 abolishes the effects of lncRNA-HEIH on CRC tumorigenesis.
Conclusion
This study demonstrated that lncRNA-HEIH promotes CRC tumorigenesis through counteracting miR-939‒mediated transcriptional repression of Bcl-xL, and suggested that lncRNA-HEIH may serve as a prognostic biomarker and therapeutic target for CRC.

Citations

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TRIM29 Overexpression Promotes Proliferation and Survival of Bladder Cancer Cells through NF-κB Signaling: Shu-Tao Tan, Sheng-Ye Liu, Bin Wu; Cancer Res Treat. 2016;48(4):1302-1312. Published online March 11, 2016; DOI: https://doi.org/10.4143/crt.2015.381

Abstract PDF PubReader ePub

Purpose
TRIM29 overexpression has been reported in several human malignancies and showed correlation with cancer cell malignancy. The aim of the current study is to examine its clinical significance and biological roles in human bladder cancer tissues and cell lines. Materials and Methods A total of 102 cases of bladder cancer tissues were examined for TRIM29 expression by immunohistochemistry. siRNA and plasmid transfection were performed in 5637 and BIU- 87 cell lines. Cell Counting Kit-8, flow cytometry, western blot, and real-time polymerase chain reaction were performed to examine its biological roles and mechanism in bladder cancer cells.
Results
We found that TRIM29 overexpression showed correlation with invading depth (p=0.0087). Knockdown of TRIM29 expression in bladder cancer cell line 5637 inhibited cell growth rate and cell cycle transition while its overexpression in BIU-87 cells accelerated cell proliferation and cell cycle progression. TRIM29 overexpression also inhibited cell apoptosis induced by cisplatin. In addition, we demonstrated that TRIM29 depletion decreased while its overexpression led to upregulated expression of cyclin D1, cyclin E, and Bcl-2. We also showed that TRIM29 knockdown inhibited protein kinase C (PKC) and nuclear factor κB (NF-κB) signaling while its overexpression stimulated the PKC and NF-κB pathways. BAY 11-7082 (NF-κB inhibitor) partly attenuated the effect of TRIM29 on expression of cyclin and Bcl-2. Treatment with PKC inhibitor staurosporine resulted in ameliorated TRIM29 induced activation of NF-κB. Conclusion The current study demonstrated that TRIM29 upregulates cyclin and Bcl family proteins level to facilitate malignant cell growth and inhibit drug-induced apoptosis in bladder cancer, possibly through PKC–NF-κB signaling pathways.

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The Chemopreventive Effect of Retinoids on Cellular NF-κB Activity Induced by NMU and NEU in Human Malignant Keratinocytes: Ki-Young Moon; Cancer Res Treat. 2007;39(2):82-87. Published online June 30, 2007; DOI: https://doi.org/10.4143/crt.2007.39.2.82

Abstract PDF PubReader ePub

Purpose

Retinoids have been shown to be effective in suppressing tumor development when chemical carcinogens such as N-nitroso-N-methylurea (NMU) and N-nitroso-N-ethylurea (NEU) were used to induce mammary tumors in a variety of animal models. However, the molecular mechanisms associated with the retinoid-mediated chemopreventive process, as linked to transcription factor NF-κB activation, for chemoprevention have not been elucidated. The purpose of this study was to determine the implications of NF-κB activation on the chemopreventive role of retinoids and their effect on cellular NF-κB activity that's induced by known alkylating chemical carcinogens such as NMU and NEU in human transfectant squamous cell carcinoma (SCC-13) cells.

Materials and Methods

The activity of NF-κB, as regulated by chemical carcinogens and retinoids, was determined in cultured human SCC-13 keratinocytes that were transfected with the pNF-κB-SEAP-NPT plasmid; this permitted the expression of the secretory alkaline phosphatase (SEAP) reporter gene in response to the NF-κB activity, and the plasmid contained the neomycin phosphotransferase (NPT) gene, which confers resistance to geneticin. The reporter enzyme activity was measured using a fluorescence detection assay method.

Results

All-trans retinoic acid and 13-cis retinoic acid induced a reduction of NF-κB activity up to 64% and 65%, respectively, compared to the control. For the treatment of the human transfectant cells with chemical carcinogens, all-trans retinoic acid (5 mM) and 13-cis retinoic acid (5 mM) downregulated the cellular NF-κB activation up to 83% and 85% compared to the NF-κB activity that was upregulated by NMU (5µM) and NEU (5µM), respectively.

Conclusion

These results suggest that the chemopreventive effect of retinoids may be mediated by the downregulated activation of NF-κB and that retinoids are implicated in the activation of NF-κB in human skin cells.

Citations

Citations to this article as recorded by

Upregulation of Nitric Oxide Synthase Activity by All-transRetinoic Acid and 13-cisRetinoic Acid in Human Malignant Keratinocytes
Ki-Young Moon
Biomedical Science Letters.2019; 25(2): 196. CrossRef
N-nitroso-N-methylurea and N-nitroso-N-ethylurea Decrease in Nitric Oxide Production in Human Malignant Keratinocytes
Ki-Young Moon
Biomedical Science Letters.2018; 24(1): 50. CrossRef
Inhibitory Effect of Retinoids on Alkaline Phosphatase Isoenzymes Activity in Human Serum
Seung Hee Kim, Ki-Young Moon
Biomedical Science Letters.2017; 23(3): 230. CrossRef
Targeting Neuroblastoma Stem Cells with Retinoic Acid and Proteasome Inhibitor
Barbara Hämmerle, Yania Yañez, Sarai Palanca, Adela Cañete, Deborah J. Burks, Victoria Castel, Jaime Font de Mora, Yiqun G. Shellman
PLoS ONE.2013; 8(10): e76761. CrossRef
Retinoids: novel immunomodulators and tumour‐suppressive agents?
MR Carratù, C Marasco, G Mangialardi, A Vacca
British Journal of Pharmacology.2012; 167(3): 483. CrossRef
Acrolein, an I-κBα-independent downregulator of NF-κB activity, causes the decrease in nitric oxide production in human malignant keratinocytes
Ki-Young Moon
Archives of Toxicology.2011; 85(5): 499. CrossRef
N-nitroso-N-methylurea and N-nitroso-N-ethylurea induce upregulation of cellular NF-κ B activity through protein kinase C-dependent pathway in human malignant keratinocytes
Ki-Young Moon
Archives of Pharmacal Research.2010; 33(1): 133. CrossRef

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