Evaluation of the Oncogene Function of GOLPH3 and Correlated Regulatory Network in Lung Adenocarcinoma

Zhang, Tong; Wang, Yue; Chen, Yangyang; Jin, Shuo; Gao, Ying; Zhang, Dan; Wu, Yang‐Chang

doi:10.3389/fonc.2021.669684

Cited by 3 publications

(2 citation statements)

References 57 publications

(59 reference statements)

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“…These lncRNAs serve the following four key roles: signaling (acting as indicators of transcriptional activity), guiding (recruiting chromatin-modifying enzymes to specific genes for remodeling or epigenetic regulation), decoying (serving as “miRNA sponges” to sequester miRNAs that target transcription factors or protein factors away from chromatin to the nucleus), and scaffolding (mediating stability of ribonucleoprotein complexes). Recent reports indicate lncRNA involvement in the regulation of GOLPH3 as well [ 44 ].…”

Section: Reviewmentioning

confidence: 99%

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Exploring the Implications of Golgi Apparatus Dysfunction in Bone Diseases

Iacobescu,

Corlatescu,

Popa

et al. 2024

Cureus

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The Golgi apparatus is an organelle responsible for protein processing, sorting, and transport in cells. Recent research has shed light on its possible role in the pathogenesis of various bone diseases. This review seeks to explore its significance in osteoporosis, osteogenesis imperfecta, and other bone conditions such as dysplasias. Numerous lines of evidence demonstrate that perturbations to Golgi apparatus function can disrupt post-translational protein modification, folding and trafficking functions crucial for bone formation, mineralization, and remodeling. Abnormalities related to glycosylation, protein sorting, or vesicular transport in Golgi have been associated with altered osteoblast and osteoclast function, compromised extracellular matrix composition, as well as disrupted signaling pathways involved with homeostasis of bones. Mutations or dysregulation of Golgi-associated proteins, including golgins and coat protein complex I and coat protein complex II coat components, have also been implicated in bone diseases. Such genetic alterations may disrupt Golgi structure, membrane dynamics, and protein transport, leading to bone phenotype abnormalities. Understanding the links between Golgi apparatus dysfunction and bone diseases could provide novel insights into disease pathogenesis and potential therapeutic targets. Future research should focus on unraveling specific molecular mechanisms underlying Golgi dysfunction associated with bone diseases to develop targeted interventions for restoring normal bone homeostasis while decreasing clinical manifestations associated with these issues.

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Section: Reviewmentioning

confidence: 99%

“…TUG1 is a recently identified oncogenic lncRNA that exhibits abnormal upregulation across various cancer types. Notably, TUG1 was significantly overexpressed in colorectal cancer patients and served as an oncogene in osteosarcoma by competitively binding with miR-335-5p [44,46]. [28,31,32,36,38,45].…”

Section: Golgi Complex and Bone Cancermentioning

confidence: 99%

Exploring the Implications of Golgi Apparatus Dysfunction in Bone Diseases

Iacobescu,

Corlatescu,

Popa

et al. 2024

Cureus

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GOLPH3‐STIP1 Complex Activates STAT3 Through Exosome Secretion to Induce Colon Cancer Metastasis

Guo,

Hong,

Huang

et al. 2024

Biotechnology Journal

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With a high mortality rate, colon cancer (CC) is the third most common malignant tumor worldwide. The primary causes are thought to be the high invasiveness and migration of CC cells. The functions of Golgi phosphoprotein 3 (GOLPH3), stress‐induced phosphoprotein 1 (STIP1), and the signal transducer and activator of transcription 3 (STAT3) signaling pathway in the invasion and migration of CC cells were examined in this study. We collected the exosomes by high‐speed centrifugation. The expressions of GOLPH3, STIP1, and epithelial‐mesenchymal transition (EMT)‐related proteins in CC tissues, cells, and exosomes were analyzed using Western blotting (WB) experiments. The abilities of CC cell invasion and migration were evaluated by the Transwell assay. The binding relationship between GOLPH3 and STIP1 was validated through Co‐immunoprecipitation (Co‐IP), and their sublocalization in CC cells was determined by immunofluorescence detection under laser confocal microscopy. Immunohistochemistry (IHC) experiments detected the expression levels of each protein in the transplanted tumor mass. Animal experiments confirmed the impact of the GOLPH3/STIP1/STAT3 regulatory axis on CC growth. We found that in CC tissues and cells, GOLPH3 was highly expressed, and silencing GOLPH3 not only greatly reduced CC cell invasion and migration but also prevented EMT. Furthermore, GOLPH3 and STIP1 interacted in CC cells, and the GOLPH3‐STIP1 complex affected the capacity for cell invasion and migration by triggering the STAT3 signaling pathway. Noteworthily, GOLPH3, and STIP1 could also be detected in CC cell exosomes, and the exosomes carried the GOLPH3‐ST1P1 complex to act on CC cells to activate intracellular STAT3 signaling, ultimately affecting the cancer cell migration and invasion. The above molecular regulatory mechanisms have also been validated in mice. In conclusion, the GOLPH3‐STIP1 complex acted on surrounding CC cells through exosomes and activated the STAT3 signaling pathway to stimulate CC cell invasion and migration.

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Down-regulation of KLRB1 is associated with increased cell growth, metastasis, poor prognosis, as well as a dysfunctional immune microenvironment in LUAD

Chen,

Wu,

Luo

et al. 2024

Sci Rep

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Killer cell lectin-like receptor B1 (KLRB1) is implicated in cancer progression and immunity. In this study, we aimed to evaluate the expression levels of KLRB1 in lung adenocarcinoma (LUAD) and analyze the relationship between KLRB1 expression levels, LUAD progression, and the tumor immune microenvironment. KLRB1 levels in LUAD were analyzed using data from the TCGA and XENA databases. Additionally, the diagnostic values of KLRB1 were analyzed in patients with LUAD. Survival and meta-analyses were employed to investigate the relationship between KLRB1 levels and other prognostic factors in patients with LUAD. Bioinformatics and cellular experiments were used to understand the functions and mechanisms of KLRB1. In addition, correlation analysis was used to investigate the relationship between KLRB1 levels and the immune microenvironment in LUAD. Reduced KLRB1 expression in LUAD was found to positively correlate with tumor size, distant metastasis, pathological stage, age, overall survival, diagnostic value, and disease-specific survival in patients with LUAD (P < 0.05). Conversely, increased KLRB1 expression was found to positively correlate with the overall survival and disease-specific survival in patients with LUAD (P < 0.05). We also found that the overexpression of KLRB1 can inhibit the proliferation, migration, and invasion of LUAD cells and promote apoptosis. KLRB1 was involved in immune cell differentiation, NF-kB, PD-L1, and PD-1 checkpoint pathways and others. Additionally, KLRB1 expression was linked to tumor purity, stromal, immune, and estimate scores, the levels of immune cells including B cells, CD8+ T cells, and CD4+ T cells, and immune cell markers in LUAD. Reduced KLRB1 expression has a significant positive correlation with diagnosis, poor prognosis, and immunity to cancer in patients with LUAD. KLRB1 inhibited cell proliferation and migration in patients with LUAD. These results suggest that KLRB1 may serve as a potential therapeutic target in patients with LUAD.

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Evaluation of the Oncogene Function of GOLPH3 and Correlated Regulatory Network in Lung Adenocarcinoma

Cited by 3 publications

References 57 publications

Exploring the Implications of Golgi Apparatus Dysfunction in Bone Diseases

Exploring the Implications of Golgi Apparatus Dysfunction in Bone Diseases

GOLPH3‐STIP1 Complex Activates STAT3 Through Exosome Secretion to Induce Colon Cancer Metastasis

Down-regulation of KLRB1 is associated with increased cell growth, metastasis, poor prognosis, as well as a dysfunctional immune microenvironment in LUAD

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