Protein kinase D2 promotes the proliferation of glioma cells by regulating Golgi phosphoprotein 3

Zhou, Xiuping; Xue, Peng; Yang, Minglin; Shi, Hengliang; Lu, Dongsi; Wang, Zhaohao; Shi, Qiong; Hu, Jinxia; Xie, Shao; Zhan, Wenjian; Yu, Rutong

doi:10.1016/j.canlet.2014.09.008

Cited by 26 publications

(26 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The protein levels of this kinase directly influence both GOLPH3 and AKT protein levels in a proportional way, i.e., high PKD2 levels correspond to high GOLPH3 and AKT levels, and vice versa. In this scenario, artificially inverting the proportionality of GOLPH3 with respect to the kinase caused a partial rescue of the effects of PKD2 on cell growth, indicating that (i) PKD2 is an upstream effector of GOLPH3 protein in regulating AKT activity; (ii) PKD2 could increase the level of GOLPH3 by modulating the PI3K-AKT signaling pathway in vitro; and (iii) the PKD2-GOLPH3-AKT signaling pathway might be a potential glioma therapeutic target [64]. Another piece of information about the role of GOLPH3 in glioma cell proliferation came from Zhou and collaborators [65].…”

Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 99%

“…Beyond invasiveness, also cell growth in gliomas is deeply influenced by GOLPH3. Zhou and collaborators [64] reported that protein kinase D2 (PKD2) upregulation promotes glioma cell proliferation (U251 and U87 cell lines), while its downregulation causes the opposite effects. The protein levels of this kinase directly influence both GOLPH3 and AKT protein levels in a proportional way, i.e., high PKD2 levels correspond to high GOLPH3 and AKT levels, and vice versa.…”

Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 99%

See 1 more Smart Citation

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Sechi

Frappaolo

Karimpour-Ghahnavieh

et al. 2020

IJMS

View full text Add to dashboard Cite

Golgi phosphoprotein 3 (GOLPH3), a Phosphatidylinositol 4-Phosphate [PI(4)P] effector at the Golgi, is required for Golgi ribbon structure maintenance, vesicle trafficking and Golgi glycosylation. GOLPH3 has been validated as an oncoprotein through combining integrative genomics with clinopathological and functional analyses. It is frequently amplified in several solid tumor types including melanoma, lung cancer, breast cancer, glioma, and colorectal cancer. Overexpression of GOLPH3 correlates with poor prognosis in multiple tumor types including 52% of breast cancers and 41% to 53% of glioblastoma. Roles of GOLPH3 in tumorigenesis may correlate with several cellular activities including: (i) regulating Golgi-to-plasma membrane trafficking and contributing to malignant secretory phenotypes; (ii) controlling the internalization and recycling of key signaling molecules or increasing the glycosylation of cancer relevant glycoproteins; and (iii) influencing the DNA damage response and maintenance of genomic stability. Here we summarize current knowledge on the oncogenic pathways involving GOLPH3 in human cancer, GOLPH3 influence on tumor metabolism and surrounding stroma, and its possible role in tumor metastasis formation.

show abstract

Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 99%

Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 99%

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Sechi

Frappaolo

Karimpour-Ghahnavieh

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Even though PKD2 has been shown to promote proliferation in other cancer cells like colorectal cancer [75] and glioma [76], the exact mechanisms by which PKD2 promotes cancer cell growth are still elusive.…”

Section: Roles Of Pkd Isoforms In Invasive Breast Cancermentioning

confidence: 99%

Functional and therapeutic significance of protein kinase D enzymes in invasive breast cancer

Durand

Borgés

Störz

2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

The Protein Kinase D (PKD) family members, PKD1, PKD2 and PKD3 constitute a family of serine/threonine kinases that are essential regulators of cell migration, proliferation and protein transport. Multiple types of cancers are characterized by aberrant expression of PKD isoforms. In breast cancer PKD isoforms exhibit distinct expression patterns and regulate various oncogenic processes. In highly-invasive breast cancer, the leading cause of cancer-associated deaths in females, the loss of PKD1 is thought to promote invasion and metastasis, while PKD2 and upregulated PKD3 have been shown to be positive regulators of proliferation, chemoresistance and metastasis. In this review, we examine the differential expression pattern, mechanisms of regulation and contributions made by each PKD isoform to the development and maintenance of invasive breast cancer. In addition, we discuss the potential therapeutic approaches for targeting PKD in this disease.

show abstract

“…It was reported that GOLPH3 could regulate glioma cell invasion and migration through the GOLPH3-mTOR-YB1 or GOLPH3-RhoA signaling pathway [ 20 – 22 ]. In addition, the overexpression of GOLPH3 promoted the proliferation of glioma cells through the PKD2-GOLPH3-AKT signaling pathway [ 23 ]. Thus, GOLH3 may become a novel therapeutic target of glioma.…”

Section: Discussionmentioning

confidence: 99%

Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1

Tian

et al. 2016

Med Sci Monit

View full text Add to dashboard Cite

BackgroundGolgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. Our previous study showed that GOLPH3 expression in glioma tissues was related to the severity of the malignancy of the cancer. However, the mechanism by which GOLPH3 affects cell apoptosis is largely unknown. The present study was designed to explore the possible mechanism of GOLPH3 in cell apoptosis.Material/MethodsTo analyze the biological role of GOLPH3 in glioma cells, we used GOLPH3 small interference RNA in apoptosis of glioma cells. The apoptosis of glioma cells was detected by flow cytometry. The expression level of GOLPH3 and NDRG1 protein was determined by Western blot analyses and immunohistochemical staining, respectively, to evaluate their association with glioma. Tumor tissues were collected from patients with glioma. Normal cerebral tissues were acquired from cerebral trauma patients undergoing internal decompression surgery.ResultsWe confirm that the decrease of GOLPH3 that promotes the apoptosis of glioma cells may be regulated by the activation of NDRG1 and cleaved capcase 3. There was a inverse association between GOLPH3 and NDRG1 in glioma samples.ConclusionsOur findings indicate that GOLPH3 and NDRG1 both play an important role in glioma etiology. Either GOLPH3 or NDRG1 might be a potential candidate for malignant glioma therapy.

show abstract

Protein kinase D2 promotes the proliferation of glioma cells by regulating Golgi phosphoprotein 3

Cited by 26 publications

References 36 publications

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Functional and therapeutic significance of protein kinase D enzymes in invasive breast cancer

Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1

Contact Info

Product

Resources

About