PRL-3 improves colorectal cancer cell proliferation and invasion through IL-8 mediated glycolysis metabolism

Xu, Hui; Zeng, Yujie; Liu, Lu; Gao, Qian; Jin, Shaowen; Lan, Qing; Wei, Lai; Luo, Xingxi; Wu, Heng; Huang, Yong‐Liang; Chu, Zhonghua

doi:10.3892/ijo.2017.4090

Cited by 32 publications

(28 citation statements)

References 34 publications

(35 reference statements)

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“…This indicates that PTP4A3 was related to the inhibition of cell proliferation caused by 1,4-BQ. The results agree with previous reports that PTP4A3 was involved in cell proliferation [28,29].…”

Section: Discussionsupporting

confidence: 93%

“…A gentle growing rate of ROS was observed in K562-PTP4A3 − cells, while a sharp increase was seen in K562-NC cells after the treatment of 20 µM 1,4-BQ. Overexpression of PTP4A3 was found to reduce the intercellular ROS level in colorectal cancer cells [28]. Further investigations are needed to explain the relationship between PTP4A3 and ROS.…”

Section: Discussionmentioning

confidence: 95%

“…The suppression of PTP4A3 induced growth inhibition of the prostate cancer cell lines in vitro [26,27]. Other studies showed that overexpression of PTP4A3 promoted cancer cell proliferation [28,29]. PI3Ks are a family of enzymes related to several cellular functions, including cell proliferation and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

Sun

et al. 2020

IJERPH

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Benzene, a commonly used chemical, has been confirmed to specifically affect the hematopoietic system as well as overall human health. PTP4A3 is overexpressed in leukemia cells and is related to cell proliferation. We previously found that HIF-1alpha was involved in benzene toxicity and PTP4A3 may be the target gene of HIF-1alpha via ChIP-seq. The aim of this study is to confirm the relationship between HIF-1alpha and PTP4A3 in benzene toxicity, as well as the function of PTP4A3 on cell toxicity induced by 1,4-benzoquinone (1,4-BQ). Our results indicate that HIF-1alpha could regulate PTP4A3 with in vivo and in vitro experiments. A cell line with suppressed PTP4A3 was established to investigate the function of PTP4A3 in 1,4-BQ toxicity in vitro. The results revealed that cell proliferation inhibition was more aggravated in PTP4A3 low-expression cells than in the control cells after 1,4-BQ treatment. The relative oxygen species (ROS) significantly increased in cells with inhibited PTP4A3, while the rise was inferior to the control cells at the 20 μM 1,4-BQ group. An increase in DNA damage was seen in PTP4A3 down-regulated cells at the 10 μM 1,4-BQ group, whereas the results reversed at the concentration of 20 μM. Moreover, the apoptosis rate increased higher in down-regulated PTP4A3 cells after 1,4-BQ exposure. In addition, PI3K/AKT pathway was significantly restrained in cells with inhibited PTP4A3 after 1,4-BQ treatment. Our results indicate that HIF-1alpha may regulate PTP4A3 to be involved in benzene toxicity. Inhibition of PTP4A3 could aggravate cell proliferation suppression and apoptosis by regulating PI3K/AKT pathway after 1,4-BQ treatment.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

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PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

Sun

et al. 2020

IJERPH

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“…PRL-3-It was reported that when colorectal cancer cells (LoVo cell line) overexpress, this phosphatase had an increase of glucose consumption and lactate production in comparison to LoVo cell line wild type. Accordingly, high amount of HK2, PKM2, and LDH were detected when PRL-3 is overexpressed [10]. Importantly, these authors also reported similar results when patient colorectal carcinoma samples were screened.…”

Section: Ptps and Warburg Effectsupporting

confidence: 59%

Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

Ferreira-Halder¹,

Clerici²,

Faria³

et al. 2020

Tumor Progression and Metastasis

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Reversible phosphorylation of proteins, executed by kinases and phosphatases, is the major posttranslational protein modification in eukaryotic cells, causing them to become activated or deactivated. This intracellular event represents a critical regulatory mechanism of several signaling pathways and can be related to a broad number of diseases, including cancer. Few decades ago, protein tyrosine phosphatases (PTPs) were considered as tumor suppressors. However, nowadays, accumulating evidence demonstrates that a misregulation of PTP activities plays a crucial and decisive role in cancer progression and metastasis. In this chapter, we will focus on the molecular aspects that support the crucial role of PTPs in cancer and in turn make them promising for prediction, monitoring, and rational appropriate therapy selection of individual patients.

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“…Hence, glucose consumption, lactate production and the ratio of ATP/ADP are usually deemed as the indexes of glycolysis (Liu et al 2016). In addition, a number of enzymes are involved in the glycolysis process, including HK2, GLUT1, LDHA, and so on (Wan et al 2017;Xu et al 2017). During the current report, MALAT1 knockdown decreased the glucose consumption, lactate production, and ratio of ATP/ ADP, as well as the down-regulation of HK2 and GLUT1 levels, suggesting MALAT1 generated a promoted effect on glycolysis process.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MALAT1 facilitates the tumorigenesis, invasion and glycolysis of multiple myeloma via miR-1271-5p/SOX13 axis

Liu

Feng

et al. 2020

J Cancer Res Clin Oncol

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Background Long non-coding RNAs (lncRNAs) play crucial roles in the regulation and treatment of multiple myeloma (MM). The objective of this research was to study the functional mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in MM. Methods MALAT1, microRNA-1271-5p (miR-1271-5p), and SRY-Box 13 (SOX13) levels were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis, and invasion were respectively assayed using 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), flow cytometry, and transwell assay. Glycolysis was evaluated by glucose consumption, lactate production, ATP/ADP ratio, and the detection of related enzymes. Associated proteins were measured using Western blot. Target relation was verified via dual-luciferase reporter assay. Xenograft tumor assay was implemented to study the influence of MALAT1 on MM in vivo. Results The up-regulation of MALAT1 and the down-regulation of miR-1271-5p were found in MM serums and cells. MALAT1 knockdown suppressed cell viability, invasion, and glycolysis while expedited cell apoptosis in MM cells. MALAT1 directly targeted miR-1271-5p and miR-1271-5p depression reverted the effects of MALAT1 knockdown on MM cells. SOX13 was a target of miR-1271-5p and SOX13 overexpression weakened the effects of miR-1271-5p on MM. MALAT1 indirectly modulated SOX13 expression through targeting miR-1271-5p. MALAT1 down-regulation inhibited MM growth by miR-1271-5p/SOX13 axis in vivo. Conclusion LncRNA MALAT1 expedited MM tumorigenesis, invasion, and glycolysis via miR-1271-5p/SOX13 axis. MALAT1 might contribute to the therapy of MM as a promising indicator.

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PRL-3 improves colorectal cancer cell proliferation and invasion through IL-8 mediated glycolysis metabolism

Cited by 32 publications

References 34 publications

PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

Long non-coding RNA MALAT1 facilitates the tumorigenesis, invasion and glycolysis of multiple myeloma via miR-1271-5p/SOX13 axis

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