Downregulation of FKBP14 by RNA interference inhibits the proliferation, adhesion and invasion of gastric cancer cells

Wang, Ruizhong; Fang, Hua; Qin, Fang

doi:10.3892/ol.2017.5781

Cited by 7 publications

(3 citation statements)

References 24 publications

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“…Herein, we initially observe that FKBP14 can effectively speed up cell growth and slow down apoptosis in the GC, which is in accordance with the study performed by Wang et al10 Using the SGC7901 cell line, we observe that KBP14 knockdown significantly inhibits cell proliferation of GC cells. Most patients die of GC as the disease has already metastasized at the time of presentation.…”

Section: Discussionsupporting

confidence: 89%

Prognostic Significance of FKBP14 in Gastric Cancer

Ghoorun¹,

Wu²,

Chen³

et al. 2019

OTT

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IntroductionAlthough our understanding on gastric cancer biology is better than a decade ago, its practical effect on screening and diagnosis remains limited. Moreover, there are no markers that can be accurately used in the clinic to diagnose early-stage gastric cancer or monitor the patient’s response to therapy. Herein, we investigate whether FKBP14 is involved in the progression of gastric cancer.MethodsThe AGS cell line was chosen for over-expression analysis, whereas the SGC-7901 cell line was selected for knock-down analysis. AGS cells were transfected with an FKBP14 overexpression plasmid (AGS-PLV.O-FLAG). The expression pattern of FKBP14 in both cell lines was determined by Western blot and RT-PCR. Cell proliferation was assessed using Cell Counting Kit-8, whereas apoptosis was performed using flow cytometry. The expression of FKBP14 in 70 Chinese patients with gastric cancer was also investigated using tissue microarrays and compared with gastric cancer patients from The Cancer Genome Atlas.ResultsFKBP14 was highly expressed in SGC7901 and had a relatively low expression in AGS cells. Upregulation of FKBP14 in AGS cells promoted migration and invasion and inhibits apoptosis. Knock-down of FKBP14 resulted in a suppression in migration and invasion and promoted apoptosis in the SGC-7901 cell line. Effectively, gastric cancer patients had a higher expression of FKBP14, with a lower survival rate (P = 0.028). Patients with a high expression of FKBP14 were significantly correlated with lymph node metastasis (P =0.016), and an advanced histologic grade (P =0.021).ConclusionFKBP14 is often up-regulated in gastric cancer. Patients with a high expression of FKBP14 are usually associated with worse overall survival. FKBP14 is an oncogene in gastric cancer, and is a potential biomarker for GC diagnosis, invasion, and prognosis.

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Section: Discussionsupporting

confidence: 89%

Prognostic Significance of FKBP14 in Gastric Cancer

Ghoorun¹,

Wu²,

Chen³

et al. 2019

OTT

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“…FKBP9 was proven to be related to poor prognoses in prostate cancer [ 27 ] and gliomas [ 28 ]. Transcriptional levels of FKBP10 and FKBP11 are upregulated in renal cell carcinoma tissues compared to normal tissues [ 13 ], and FKBP14 is involved in various types of human tumors such as gastric cancer [ 29 , 30 ], human cervical cancers [ 31 ], ovarian cancer [ 32 ], and osteosarcomas [ 33 ]. In addition, FKBP15 was verified to be upregulated in breast cancer patients [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

Penetrating Exploration of Prognostic Correlations of the FKBP Gene Family with Lung Adenocarcinoma

Wang

Shen

Anuraga

et al. 2022

JPM

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The complexity of lung adenocarcinoma (LUAD), the development of which involves many interacting biological processes, makes it difficult to find therapeutic biomarkers for treatment. FK506-binding proteins (FKBPs) are composed of 12 members classified as conservative intracellular immunophilin family proteins, which are often connected to cyclophilin structures by tetratricopeptide repeat domains and have peptidyl prolyl isomerase activity that catalyzes proline from residues and turns the trans form into the cis form. Since FKBPs belong to chaperone molecules and promote protein folding, previous studies demonstrated that FKBP family members significantly contribute to the degradation of damaged, misfolded, abnormal, and foreign proteins. However, transcript expressions of this gene family in LUAD still need to be more fully investigated. In this research, we adopted high-throughput bioinformatics technology to analyze FKBP family genes in LUAD to provide credible information to clinicians and promote the development of novel cancer target drugs in the future. The current data revealed that the messenger (m)RNA levels of FKBP2, FKBP3, FKBP4, FKBP10, FKBP11, and FKBP14 were overexpressed in LUAD, and FKBP10 had connections to poor prognoses among LUAD patients in an overall survival (OS) analysis. Based on the above results, we selected FKBP10 to further conduct a comprehensive analysis of the downstream pathway and network. Through a DAVID analysis, we found that FKBP10 was involved in mitochondrial electron transport, NADH to ubiquinone transport, mitochondrial respiratory chain complex I assembly, etc. The MetaCore pathway analysis also indicated that FKBP10 was involved in "Ubiquinone metabolism", "Translation_(L)-selenoaminoacid incorporation in proteins during translation", and "Transcription_Negative regulation of HIF1A function". Collectively, this study revealed that FKBP family members are both significant prognostic biomarkers for lung cancer progression and promising clinical therapeutic targets, thus providing new targets for treating LUAD patients.

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“…A previous report has elucidated that FKBP14 overexpression promotes the growth of osteosarcoma cells 6. Moreover, FKBP14 silencing has reduced the proliferation, adhesion and invasion of gastric and ovarian cancer cells, respectively 7,8. Nevertheless, the biological role of FKBP14 is still unclear in colon carcinoma cells.…”

Section: Introductionmentioning

confidence: 99%

FKBP14 Promotes The Proliferation And Migration Of Colon Carcinoma Cells Through Targeting IL-6/STAT3 Signaling Pathway

Yang

Zhang

Yang

et al. 2019

OTT

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PurposeFK506-binding proteins 14 (FKBP14), a highly conserved protein, is identified as an oncogene in certain human tumors. However, the detailed biological function of FKBP14 in colon carcinoma remains unclear. The purpose of the present research is to examine the role of FKBP14 in human colon carcinoma cells.MethodsIn the present study, FKBP14 induced silencing and overexpression in colon carcinoma cells by using RNA interference (RNAi) and lentiviral vector, respectively. A specific JAK/STAT inhibitor AG490 was used to explore the relationship between FKBP14 and STAT3 in colon carcinoma cells. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to examine the level of FKBP14 in colon carcinoma cells. Cell counting kit-8 (CCK-8) assay was used to determine the proliferation rate of colon carcinoma cells. Further, the migration rate of colon carcinoma cells was analyzed by performing a migration assay.ResultsOur results demonstrated that FKBP14 was upregulated in human colon carcinoma tissues. Moreover, high level of FKBP14 was associated with poor prognosis of colon carcinoma patients. Further, our findings firstly elucidated that FKBP14 was a pro-proliferation and migration factor in colon carcinoma cells. More importantly, FKBP14 might be a novel component in IL-6/JAK/STAT3 pathway and targeted STAT3 in colon carcinoma cells.ConclusionOur research not only indicated the potential signaling pathway of FKBP14 in colon carcinoma cells but also provided novel insight into the treatment for colon carcinoma.

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Downregulation of FKBP14 by RNA interference inhibits the proliferation, adhesion and invasion of gastric cancer cells

Cited by 7 publications

References 24 publications

<p>Prognostic Significance of FKBP14 in Gastric Cancer</p>

<p>Prognostic Significance of FKBP14 in Gastric Cancer</p>

Penetrating Exploration of Prognostic Correlations of the FKBP Gene Family with Lung Adenocarcinoma

<p>FKBP14 Promotes The Proliferation And Migration Of Colon Carcinoma Cells Through Targeting IL-6/STAT3 Signaling Pathway</p>

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