<i>PAR-2</i> promotes cell proliferation, migration, and invasion through activating PI3K/AKT signaling pathway in oral squamous cell carcinoma

Tang, Kailiang; Han-Ying, Tang; Du, Yi; Tian, Tian; Xiong, Sheng

doi:10.1042/bsr20182476

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…21,22 The levels of P-PI3K and P-AKT are vital indicators of the activity of the PI3K/AKT signaling pathway, which is associated with aggressive tumor cell behaviors in OSCC, such as proliferation, angiogenesis, metastasis, and chemoresistance. [23][24][25] Interestingly, we found that P-PI3K and P-AKT levels were predominantly weakened in SCC-4…”

Section: Discussionmentioning

confidence: 72%

miR‐186‐5p inhibits the progression of oral squamous cell carcinoma by targeting ITGA6 to impair the activity of the PI3K/AKT pathway

Min

Zhang

2022

J Oral Pathology Medicine

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Background microRNAs (miRNAs) are pivotal regulators of multiple biological processes. miR‐186‐5p functions as a tumor suppressor in a variety of cancers and promotes the malignant proliferation of oral squamous cell carcinoma (OSCC). This study aimed to clarify the role and regulatory mechanism of miR‐186‐5p in OSCC. Methods The levels of miR‐186‐5p and integrin subunit alpha 6 (ITGA6) were investigated in clinical specimens and OSCC cell lines by reverse transcription‐quantitative polymerase chain reaction. The effects of miR‐186‐5p and ITGA6 on the cell migration, proliferation, and phosphatidylinositol 3‐kinase (PI3K)/serine‐threonine kinase (AKT) pathway activity were evaluated by transwell assay, cell counting kit 8 assay, and western blotting, respectively. A xenograft model was used to analyze the effect of miR‐186‐5p on tumor growth. Bioinformatic analyses were conducted to identify the putative targets of miR‐186‐5p in OSCC. Results Decreased miR‐186‐5p expression levels were observed in OSCC tumor tissues and cell lines. The overexpression of miR‐186‐5p suppressed the proliferation and migration of OSCC cells, and weakened the phosphorylation of PI3K and AKT. Moreover, the overexpression of miR‐186‐5p in xenograft tumor models impedes tumor growth. miR‐186‐5p is bound to ITGA6 and negatively related to ITGA6 expression in tumor tissues. The forced expression of ITGA6 promoted OSCC cell proliferation and migration and enhanced the phosphorylation levels of PI3K and AKT, while additional miR‐186‐5p enrichment partly abolished these effects. Conclusion miR‐186‐5p binds to ITGA6 to impair the activity of the PI3K/AKT signaling pathway, thereby blocking the development of OSCC. This study provides insight to understand the pathogenesis of OSCC.

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Section: Discussionmentioning

confidence: 72%

miR‐186‐5p inhibits the progression of oral squamous cell carcinoma by targeting ITGA6 to impair the activity of the PI3K/AKT pathway

Min

Zhang

2022

J Oral Pathology Medicine

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“…The PI3K/AKT signaling pathway is related to a variety of human malignant tumor biological processes, such as cell adhesion, growth, invasion, and angiogenesis (34,35). The PI3K/AKT pathway is one of the most common activation pathways in cancers, and it is of great significance in regulating glucose metabolism, proliferation and apoptosis of tumor cells (36). Akt plays a role in the anti-apoptotic pathway through phosphorylation of downstream target proteins.…”

Section: Discussionmentioning

confidence: 99%

CaMKKβ regulates proliferation, apoptosis, and glycolysis of hepatocellular carcinoma via PI3K/AKT pathway

Sheng¹,

Mao²,

Zhang³

2020

Ann Palliat Med

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Background: Hepatocellular carcinoma (HCC) is the most common malignancy of liver cancer. Calcium ions/calmodulins stimulate protein kinase kinases β (CaMKKβ) is a multifunctional protein kinase that is overexpressed in many types of cancer. This study aims to investigate the effect of CaMKKβ interference on HCC in HepG2 cells and transplanted tumor mice.Methods: CaMKKβ gene was knocked out in HepG2 cells as an experimental group, empty vector lentivirus as a negative control (NC) group, and untreated HepG2 cells as a control group. Cell proliferation, cell cycle, apoptosis, invasion, and glycolysis potential assays were conducted, respectively. In addition, the expression of PI3K, p-PI3K, AKT, and p-AKT was quantified by Western blot. Finally, the effect of CaMKKβ in vivo was investigated using a xenograft model. Results: CaMKKβ knockdown significantly suppressed HepG2 cell proliferation, cell cycle, invasion, EMT, and glycolysis, promoted cell apoptosis, and reduced the expression of hexokinase 2 (HK2), pyruvate kinase M (PKM2), and lactate dehydrogenase A (LDHA), p-PI3K, and p-AKT. Post the addition of AKT highly expression plasmid, glucose uptake, lactic acid production, and cell proliferation decreased, accompanied by an increase in apoptosis, which were substantially reversed. Notably, xenograft model experiments in vivo also confirmed that CaMKKβ knockdown inhibited HCC growth.Conclusions: CaMKKβ knockdown inhibited cell proliferation, invasion, and glycolysis through the PI3K/AKT pathway, heightened apoptosis, thus promoting the development of HCC. This might be a potential target for the diagnosis and treatment of HCC.

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“…The PARs are a family of G-Protein coupled Receptors that are often described as coagulation sensors, since their mode of action includes a proteolysis step induced by thrombin or other coagulation proteases. The expression of PAR2 was recently reported to transduce mitogenic and proinvasive signals in OSCC cells [ 27 , 28 ]. The activation of PAR2 may directly boost tumor growth after surgery.…”

Section: Key Perioperative Events and The Relevant Biological Parametersmentioning

confidence: 99%

Therapeutic Perspectives for the Perioperative Period in Oral Squamous Cell Carcinoma (OSCC)

Galmiche¹,

Saidak²,

Bettoni³

et al. 2022

Front. Oral. Health

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The perioperative period is the relatively short window of time, usually measured in days or weeks, around the surgical procedure. Despite its short duration, this time period is of great importance for cancer patients. From a biological point of view, the perioperative period is complex. Synchronous with primary tumor removal, surgery has local and distant consequences, including systemic and local inflammation, coagulation and sympathetic activation. Furthermore, the patients often present comorbidities and receive several medical prescriptions (hypnotics, pain killers, anti-emetics, hemostatics, inotropes, antibiotics). Because of the complex nature of the perioperative period, it is often difficult to predict the oncological outcome of tumor resection. Here, we review the biological consequences of surgery of Oral Squamous Cell Carcinoma (OSCC), the most frequent form of primary head and neck tumors. We briefly address the specificities and the challenges of the surgical care of these tumors and highlight the biological and clinical studies that offer insight into the perioperative period. The recent trials examining neoadjuvant immunotherapy for OSCC illustrate the therapeutic opportunities offered by the perioperative period.

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PAR-2 promotes cell proliferation, migration, and invasion through activating PI3K/AKT signaling pathway in oral squamous cell carcinoma

Cited by 13 publications

References 25 publications

miR‐186‐5p inhibits the progression of oral squamous cell carcinoma by targeting ITGA6 to impair the activity of the PI3K/AKT pathway

miR‐186‐5p inhibits the progression of oral squamous cell carcinoma by targeting ITGA6 to impair the activity of the PI3K/AKT pathway

CaMKKβ regulates proliferation, apoptosis, and glycolysis of hepatocellular carcinoma via PI3K/AKT pathway

Therapeutic Perspectives for the Perioperative Period in Oral Squamous Cell Carcinoma (OSCC)

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