Pyrroline-5-Carboxylate Reductase 1 Accelerates the Migration and Invasion of Nonsmall Cell Lung Cancer <i>In Vitro</i>

Sang, Senhua; Zhang, Cuicui; Shan, Jianwei

doi:10.1089/cbr.2019.2782

Cited by 19 publications

(14 citation statements)

References 41 publications

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“…It have been demonstrated that a wide array of proteins were involved in the tumorigenesis, progress, metastasis, and drug-resistance of lung cancer [17][18][19]. Among those molecules, PYCR1 represents one of the most seductive proteins because overexpression of PYCR1 was suggested to be the most related factor that contributed to poor outcomes of patients with malignant cancer [11][12][13]. In the present study, we demonstrated that the levels of PYCR1 was signi cantly higher in lung cancer tissues and cells than of the tumor adjacent normal tissues and normal cells.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, over expression of PYCR1 was detected in breast cancer and down-regulation of PYCR1 levels markedly decrease the proliferation ability of breast cancer cells, while obviously enhanced the apoptosis rate of cancer cells [10]. Importantly, high level of PYCR1 was also detectable in NSCLC and it was high expression of PYCR1 closely related to the progression of NSCLC [11]. However, the aberrant expression of PYCR1 in NSCLC and its role and mechanisms in regulating progress of lung cancer are still need to be thoroughly investigated, so as to provide a new theoretical basis for the diagnosis and treatment of lung cancer.…”

Section: Introductionmentioning

confidence: 95%

“…Pyrroline-5-carboxylate reductase 1 (PYCR1), an enzyme involved in cell metabolism, has been shown to be up-regulated in many cancer types [9][10][11][12]. Previous study has proved that knockdown of PYCR1 signi cantly inhibited the proliferation, colony, and invasion of prostate cancer cells [9].…”

Section: Introductionmentioning

confidence: 99%

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WITHDRAWN: PYCR1 Promotes Proliferation, Invasion and Drug-Resistance of Lung Cancer Cells by Regulating STAT3-Mediated PI3K/AKT and NF-κB Signaling Pathway

Yu¹,

Wang²,

Zhang³

et al. 2020

Preprint

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Abstract Background: Aberrant expression of PYCR1 has been proved to be one of the most pivotal regulators of tumor progress and metastasis. However, the detailed role of PYCR1 in promotion of NSCLC progress is not investigated thoroughly. The present study was aimed to thoroughly investigate the effect of PYCR1 in the growth of NSCLC and the underlying mechanisms, so that provide valuable theoretical basis for efficient treatment of NSCLC. Methods: The expressions of PYCR1 and its target genes and downstream signals were respectively determined by Western-blot assay and RT-qPCR experiment. Cell growth of NSCLC cells was investigated using the CCK-8 kit while the proliferation assay was performed with the help of EDU staining. The NSCLC-bearing mice mode was established to evaluate the effect of PYCR1 on the progress of NSCLC and the underlying mechanisms in vivo.Results: It was firstly demonstrated that the PYCR1 was overexpressed in lung cancer tissues and cells and overexpression of PYCR1 contributed to significantly enhanced proliferation, invasion, and drug-resistance of cancer cells and progress of NSCLC tissues. Further studies revealed that up-regulation of PYCR1 level resulted to the elevation of bioactivity of STAT3. Additionally, the positive correlation between the expression of PYCR1 and STAT3 indicated that the PYCR1 promotes the growth of NSCLC through targeting regulation the STAT3 levels. Furthermore, activation of STAT3 by PYCR1 was proved to be able of awaking the PI3K/AKT and NF-κB signaling pathway, which was extremely important to the metabolism, proliferation, cell survival, and growth of many cancer cell types.Conclusion: In conclusion, our study demonstrated that PYCR1 was specifically overexpressed in lung cancer and closely related to rapid progress and drug-resistance thorough regulating the STAT3-mediated PI3K/AKT and NF-κB signaling pathway. It may provide a valuable strategy for treatment of malignant lung cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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WITHDRAWN: PYCR1 Promotes Proliferation, Invasion and Drug-Resistance of Lung Cancer Cells by Regulating STAT3-Mediated PI3K/AKT and NF-κB Signaling Pathway

Yu¹,

Wang²,

Zhang³

et al. 2020

Preprint

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“…Increased expression of PYCR1 has since been confirmed in different cancers, including melanoma, NSCLC, renal cell carcinoma, breast cancer, colorectal cancer, prostate cancer, hepatocellular carcinoma, and isocitrate dehydrogenase 1 (IDH1)-mutant gliomas 41,42,64,[96][97][98][99][100][101][102] . In some instances, PYCR1 expression is a reliable diagnostic biomarker which predicts poor prognosis in patients with melanoma 96 , breast cancer 64,101 , renal cell cancers 100,103 , and NSCLC 98 .…”

Section: The Ambivalent Role Of Prodh In Cancermentioning

confidence: 99%

The Janus-like role of proline metabolism in cancer

et al. 2020

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The metabolism of the non-essential amino acid L-proline is emerging as a key pathway in the metabolic rewiring that sustains cancer cells proliferation, survival and metastatic spread. Pyrroline-5-carboxylate reductase (PYCR) and proline dehydrogenase (PRODH) enzymes, which catalyze the last step in proline biosynthesis and the first step of its catabolism, respectively, have been extensively associated with the progression of several malignancies, and have been exposed as potential targets for anticancer drug development. As investigations into the links between proline metabolism and cancer accumulate, the complexity, and sometimes contradictory nature of this interaction emerge. It is clear that the role of proline metabolism enzymes in cancer depends on tumor type, with different cancers and cancer-related phenotypes displaying different dependencies on these enzymes. Unexpectedly, the outcome of rewiring proline metabolism also differs between conditions of nutrient and oxygen limitation. Here, we provide a comprehensive review of proline metabolism in cancer; we collate the experimental evidence that links proline metabolism with the different aspects of cancer progression and critically discuss the potential mechanisms involved.

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“…33 Sang et al showed that increased expression of E-cadherin and decreased expression of N-cadherin in nonsmall cell lung cancer can activate EMT to enhance tumor invasion and migration. 34 Zhou et al demonstrated that E-cadherin expression in IPA is significantly lower than that in NIPA. After follow-up, E-cadherin expression in patients with pituitary adenoma recurrence was lower than that in nonrecurrence, indicating that low E-cadherin expression is closely related to the invasion and prognosis of pituitary adenomas, but which signaling pathway regulates the invasiveness of pituitary adenomas is unclear.…”

Section: Discussionmentioning

confidence: 99%

Correlation between the Expression of Interleukin-6, STAT3, E-Cadherin and N-Cadherin Protein and Invasiveness in Nonfunctional Pituitary Adenomas

Shen

Liu

et al. 2019

J Neurol Surg B Skull Base

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Objective This study aimed to investigate the expression of interleukin (IL)-6, signal transducer and activator of transcription 3 (STAT3), epithelial-cadherin (E- cadherin) and neural-cadherin (N-cadherin) proteins in nonfunctional pituitary adenomas, and their correlation with invasiveness. Method Thirty cases of nonfunctional pituitary adenoma pathological wax specimens were selected from our hospital, including 20 cases of invasive nonfunctional pituitary adenoma (INFPA) and 10 noninvasive nonfunctional pituitary adenomas (NNFPAs). Envision was used to detect IL-6, STAT3, E-cadherin , and N-cadherin in specimens. Statistical methods were used to analyze the correlation between the four proteins and the Knosp classification of nonfunctional pituitary adenomas. Result IL-6 and STAT3 were highly expressed in INFPAs but poorly expressed in NNFPAs. E-cadherin expression in INFPAs was lower than that in NNFPAs. N-cadherin was positive or strongly positive in both groups. Spearman's correlation analysis showed that the expression of IL-6 and STAT3 was positively correlated with Knosp's classification, whereas the expression of E-cadherin was negatively correlated with Knosp classification. Meanwhile, the expression of N-cadherin was not correlated with Knosp's classification. Conclusion The expression of the IL-6, STAT3, E-cadherin proteins were associated nonfunctional pituitary adenomas. However, the expression of N-cadherin was not correlated with nonfunctional pituitary adenomas.

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Pyrroline-5-Carboxylate Reductase 1 Accelerates the Migration and Invasion of Nonsmall Cell Lung Cancer In Vitro

Cited by 19 publications

References 41 publications

WITHDRAWN: PYCR1 Promotes Proliferation, Invasion and Drug-Resistance of Lung Cancer Cells by Regulating STAT3-Mediated PI3K/AKT and NF-κB Signaling Pathway

WITHDRAWN: PYCR1 Promotes Proliferation, Invasion and Drug-Resistance of Lung Cancer Cells by Regulating STAT3-Mediated PI3K/AKT and NF-κB Signaling Pathway

The Janus-like role of proline metabolism in cancer

Correlation between the Expression of Interleukin-6, STAT3, E-Cadherin and N-Cadherin Protein and Invasiveness in Nonfunctional Pituitary Adenomas

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