CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

Tu, Ming-Gene; Cai, Lin; Zheng, Wenjie; Su, Zhipeng; Chen, Yong; Qi, Songtao

doi:10.3892/mmr.2017.6204

Cited by 14 publications

(19 citation statements)

References 25 publications

(31 reference statements)

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“…Moreover, these genes were also involved in the oncogenic progression of primitive neuroectodermal tumor in IPA analysis. Another gene involved in multiple cancers, CD164, has been reported to promote glioma via the tumor-suppressor PTEN [ 119 ]. These data suggest that FOXP2 may have the capacity to repress both pro-oncogenic and tumor suppressor genes.…”

Section: Introductionmentioning

confidence: 99%

The untold stories of the speech gene, the FOXP2 cancer gene

Herrero

Gitton

2018

Genes Cancer

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FOXP2 encodes a transcription factor involved in speech and language acquisition. Growing evidence now suggests that dysregulated FOXP2 activity may also be instrumental in human oncogenesis, along the lines of other cardinal developmental transcription factors such as DLX5 and DLX6 [1–4].Several FOXP familymembers are directly involved during cancer initiation, maintenance and progression in the adult [5–8]. This may comprise either a pro-oncogenic activity or a deficient tumor-suppressor role, depending upon cell types and associated signaling pathways. While FOXP2 is expressed in numerous cell types, its expression has been found to be down-regulated in breast cancer [9], hepatocellular carcinoma [8] and gastric cancer biopsies [10]. Conversely, overexpressed FOXP2 has been reported in multiple myelomas, MGUS (Monoclonal Gammopathy of Undetermined Significance), several subtypes of lymphomas [5,11], as well as in neuroblastomas [12] and ERG fusion-negative prostate cancers [13]. According to functional evidences reported in breast cancer [9] and survey of recent transcriptomic and proteomic analyses of different tumor biopsies, we postulate that FOXP2 dysregulation may play a main role throughout cancer initiation and progression. In some cancer conditions, FOXP2 levels are now considered as a critical diagnostic marker of neoplastic cells, and in many situations, they even bear strong prognostic value [5]. Whether FOXP2 may further become a therapeutic target is an actively explored lead. Knowledge reviewed here may help improve our understanding of FOXP2 roles during oncogenesis and provide cues for diagnostic, prognostic and therapeutic analyses.

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Section: Introductionmentioning

confidence: 99%

The untold stories of the speech gene, the FOXP2 cancer gene

Herrero

Gitton

2018

Genes Cancer

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“…As a multifunctional protein, CD164 acted as a surface marker of hematopoietic stem cells, a CXCR4 promoter activity‐enhancing transcription factor, and a stem cell‐specific marker inducer 9, 10, 11. High expression of CD164 was found in several malignant diseases and was associated with clinical outcomes of patients 13, 23, 28, 29, 30, 31. In lung cancer, the positive associations were significantly existed between CD164 expression and tumor size, tumor cell grading, and lymph node involvement 14.…”

Section: Discussionmentioning

confidence: 97%

“…Previous studies have revealed that CD164 was involved in tumor progression via the regulation of cell proliferation and apoptosis in several cancers 13, 14, 15, 23, 32. In addition, CD164 was implicated in regulating the migration and invasion of lung cancer and medulloblastoma cells 17, 18.…”

Section: Discussionmentioning

confidence: 99%

“…38 In recent years, many studies have indicated that CD164 played a role in tumor progression by interacting with CXCR4 and regulating the downstream of CXCR4 pathway 23. Knocking‐down of CD164 could up‐regulate PTEN and inhibit the activities of PI3K/AKT pathway 13. Besides, CD164 promoted lung tumor‐initiating cells with stem cell activity and determined tumor growth and drug resistance through Akt/mTOR signaling pathway 14.…”

Section: Discussionmentioning

confidence: 99%

“…In human cancers, CD164 was reported played roles in many different cancers. For instance, CD164 has been reported for the maintenance and progression of human tumors, such as human glioma,13 lung cancer,14 ovarian cancer,15 and prostate cancer 16. Besides, some microRNAs such as miR‐124 and miR‐219 were found that could suppress the proliferation, migration, and invasion of tumor cells by targeting CD164 17, 18.…”

Section: Introductionmentioning

confidence: 99%

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CD164 promotes tumor progression and predicts the poor prognosis of bladder cancer

Zhang

Li³

et al. 2018

Cancer Medicine

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CD164 was found to play a role in many malignant diseases. But the roles of CD164 in human bladder cancer have not yet been studied. The object of our study was to investigate the functions of CD164 in urothelial bladder carcinoma. The immunohistochemistry (IHC) was performed to evaluate the associations between the expression level of CD164 and clinical‐pathological features of patients, and IHC was used to analyze the relationship between CD164 and CXCR4 in tumor tissues. Real‐time qPCR and Western blot were used to measure the expression of relevant genes. The roles of CD164 in tumor cells and tissues were investigated by in vitro and in vivo experiments. The results of immunohistochemistry found that CD164 was associated with clinical and pathological features of patients. High level of CD164 was related to the distant metastasis and vascular invasion of bladder cancer patients. In vitro, by silencing of CD164, the proliferation, migration, and invasion of tumor cells were inhibited significantly by regulating related proteins such as Ki67, proliferating cell nuclear antigen, matrix metalloproteinases‐2, and matrix metalloproteinases‐9. In vivo, knocking‐down of CD164 could reduce the growth and metastasis of tumors in mice. In addition, a co‐expression was found between CD164 and CXCR4 in tumor tissues. In conclusion, our study demonstrated that CD164 was associated with the poor clinical outcomes of BC patients. Silencing of CD164 could inhibit the progression of tumors in vivo and in vitro, which may become an effective target in the treatment of bladder cancer.

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Characterization of Transcriptome Transition Associates Long Noncoding RNAs with Glioma Progression

Lin

Jiang

Bai

et al. 2018

Molecular Therapy - Nucleic Acids

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Long noncoding RNAs (lncRNAs) have been implicated in cancer biogenesis and prognosis. However, we still lack knowledge on their function during glioma progression. In this study, we analyzed the lncRNA expression profile across 907 glioma patients in grades II, III, and IV. Widespread dynamic expression of lncRNAs during glioma progression was revealed, and we identified 33 onco-lncRNAs and 61 tumor suppressor lncRNAs. We found that the expression of these oncogenic lncRNAs is regulated by grade-specific expressed transcription factors. Based on the “guilt by association” rule, we predicted the potential functions of oncogenic lncRNAs, and the majority of these lncRNAs are involved in cancer hallmarks. Especially we found that CARD8-AS1 regulates the metastatic potential of glioma cell lines in vitro. Integrating clinical information, we identified the 12 protective and 8 risk lncRNAs (such as PWAR6 and CARD8-AS1) in glioma. Finally, an lncRNA-gene functional module was identified to be associated with the survival of patients. The predictive ability of this module signature was further validated in an independent dataset. Our results revealed the dynamic transcriptome transition during glioma progression, indicating that the lncRNA signature could be a useful biomarker that may improve upon our understanding of the molecular mechanisms underlying glioma progression.

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CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

Cited by 14 publications

References 25 publications

The untold stories of the speech gene, the FOXP2 cancer gene

The untold stories of the speech gene, the FOXP2 cancer gene

CD164 promotes tumor progression and predicts the poor prognosis of bladder cancer

Characterization of Transcriptome Transition Associates Long Noncoding RNAs with Glioma Progression

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