Involvement of NF-κB signaling pathway in the regulation of PRKAA1-mediated tumorigenesis in gastric cancer

Zhang, Yangmei; Zhou, Xichang; Zhang, Youwei; Wang, Xiang; Cheng, Long

doi:10.1080/21691401.2019.1657876

Cited by 14 publications

(14 citation statements)

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“…AMP-activated alpha 1 catalytic subunit (PRKAA1) is one of the subunits of the mammalian 5′-AMP-activated protein kinase (AMPK). They play a crucial role in the maintenance of intracellular energy metabolism and hence are considered as a gastric carcinoma risk factor [ 56 ]. In NF- κ Bp50 knockdown rats, H. pylori infection upregulates the expression of p-NF- κ Bp50, NF- κ Bp50, and PRKAA1 expression, which promotes carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…PRKAA1 knockdown in gastric cancer cells showed a significant decrease in cell invasion and migration. It also inhibited the expression of MMP-2 and activation of NF- κ B, whereas on the contrary, PRKAA1 involved in NF- κ Bp50 mediated gastric cancer cell invasion and migration indicated their role in gastric cell carcinogenesis [ 56 ]. H. pylori -induced inflammatory response of gastric cells leads to increased epithelial cell turnover by increasing its proliferation and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

Sheweita

Alsamghan

2020

Mediators of Inflammation

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Cancer causes a major health concern worldwide due to high incidence and mortality rates. To accomplish this purpose, the Scopus, PubMed, and Web of Science databases were searched using the keywords bacteria and cancer. Most of published research addressed several different factors that induced cancer, such as toxins, medications, smoking, and obesity. Nonetheless, few studies are dealing with cancer induction via bacterial infection. In addition, mechanisms of cancer induction via bacterial infections are not well understood. Therefore, in this review, we will shed light on different bacteria that induced cancer via different molecular mechanisms. Among the bacterial infection that induced cancer, Helicobacter pylori was the first recognized bacteria which caused gastric cancer and might be also linked to extragastric cancer in humans. H. pylori has been associated with adenocarcinoma in the distal stomach by its ability to cause severe inflammations. It has been found that inflammations induced cancer via different mechanisms including induction of cell proliferation and production of high levels of free radicals. Recently, free radicals were found to induce and cause various types of cancer. Salmonella typhi has been found to be associated with gallbladder carcinoma (GBC). Also, intercellular infection of lungs with Chlamydia pneumoniae was found to contribute as one of the ethological factors of lung cancer. Moreover, infection of the urinary tract with Staphylococcus aureus, Klebsiella spp., and Proteus mirabilis has been found to cause bladder cancer. These microorganisms produce a high level of N-nitrosamines which are metabolically activated leading to the generation of alkylating agents that damage DNA and other macromolecules. It is concluded that a certain bacterium is linked with induction of a specific type of cancer via different molecular and biochemical mechanisms as discussed in the text in details. This infection could potentially affect human health in different ways. In addition, it is important to know the possible factors involved in cancer induction for better treatment of cancer patients.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

Sheweita

Alsamghan

2020

Mediators of Inflammation

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“…The following plasmids (Shanghai GenePharma Co., Ltd.; 2.5 ng/well) were used: i) pcDNA Flag TRIP6 or shNC (non-coding shRNA)/pGPU6/GFP/Neo plasmids as the negative control; ii) TRIP6-small interfering RNA (siRNA; 5'-GAA GCT GGT TCA CGA CAT GAA-3') or TRIP6-negative control (NC); iii) pcDNA Flag P65 or shNC/pGPU6/GFP/Neo plasmids as the negative control; and iv) P65-siRNA (5'-GAA CAC AAT GGC CAC TTG CC-3') or P65-NC. After transfection, the cells were cultured for 24 Osteosarcoma was found in the following sites in patients: In the femur in 21 patients, in the tibia in 24 patients and in other sites in ten patients. The tumor diameter was <5 cm in 19 cases and ≥5 cm in 36 cases.…”

Section: Methodsmentioning

confidence: 99%

“…Extracellular signaling factors bind to receptors on the cell membrane and initiate a cascade of downstream pathways (23). Receptor proteins first activate IκB kinase (IKK) upon stimulation (24). IKK then phosphorylates serine at the regulatory site of the IκB subunit on the intracellular NF-κB/IκB compound, which allows the IκB subunit to be ubiquitinated and degraded by the proteasome to release the NF-κB dimer (25)(26)(27)(28)(29).…”

Section: Trip6 Regulates the Proliferation Migration Invasion And Amentioning

confidence: 99%

TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF‑κB signaling pathway

Liu

Cheng

et al. 2020

Exp Ther Med

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Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of the zyxin family of Lin-Isl-Mec (LIM) proteins, is an adaptor protein primarily expressed in epithelial cells. TRIP6 can regulate a variety of cellular responses, such as actin cytoskeletal reorganization and cell adhesion. However, to the best of our knowledge, the role of TRIP6 in osteosarcoma (Os) has not been previously reported. Therefore, the present study investigated the role of TRIP6 in the occurrence and development of Os, and the potential of utilizing TRIP6 as a therapeutic target in Os. The present results suggested that the expression levels of TRIP6 were significantly increased in Os cells and clinical tissue specimens compared with normal osteoblasts and adjacent non-tumor tissue. Moreover, the present results suggested that overexpressing TRIP6 significantly increased proliferation, migration and invasion, while inhibiting apoptosis in Os cells. However, silencing TRIP6 decreased proliferation, migration and invasion, while activating apoptosis in Os cells. The present results suggested that overexpression of TRIP6 increased NF-κB activation by decreasing the protein expression levels of inhibitor of κBα, and increasing total and phosphorylated P65 levels. The present results indicated that TRIP6 silencing decreased NF-κB activation. Collectively, the present results suggested that TRIP6 may play a role in promoting Os cell proliferation, migration and invasion, while inhibiting cell apoptosis. Furthermore, TRIP6 may be utilized as a novel prognostic biomarker and therapeutic target in Os.

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“…Surgery is often difficult to further embodiments gastrointestinal radical resection [2] . Selecting an effective treatment regimen depends on comprehensive evaluation before surgery, including lesion size, range, depth and the situation involving the stomach wall lymph nodes and distant metastasis, chronic and cause, clinical physiology of gastric lesion type, severity and differentiation of biological behavior of learning diagnosis is closely related [3] .…”

mentioning

confidence: 99%

Inhibitory Effect of Hydroxysafflor Yellow Pigment A on Human Gastric Adenocarcinoma BGC-823 Xenograft in Nude Mice

Mao¹,

Fang²

2021

ijps

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Mao et al.: Inhibitory Effect of HSYA on Human Gastric AdenocarcinomaIn China, the incidence rate and mortality rate of gastric cancer are in the second place among all tumors and the pathological type is mainly adenocarcinoma. The higher prevalence rate requires us to do more research. It is of great significance to study the antitumor effect of hydroxysafflor yellow pigment A in gastric adenocarcinoma. The aim of this study was to investigate the inhibitory effect of hydroxysafflor yellow pigment A on human gastric adenocarcinoma BGC-823 xenograft in nude mice. The animal model of human gastric adenocarcinoma BGC-823 was established in nude mice to carry out the experiment and then the transmission electron microscope was used to observe and analyze the experimental data. The results showed that on the 4th d after inoculation, there were more subcutaneous tumor masses in nude mice and on the 7th d, all the nude mice formed tumor blocks with the size of 0.4 cm to 0.8 cm and the tumorigenesis rate was 100 %. With the continuous administration, the tumor weight of the small dose group was only 0.88 g, which was much smaller than that of the model group. The average percentage of early apoptosis in low dose group was 2.48 % and that in model group was 0.44 %. In the low dose group, the volume of tumor cells became smaller and apoptotic bodies appeared. Therefore, it is of great significance to study the inhibitory effect of hydroxysafflor yellow pigment A on human gastric adenocarcinoma BGC-823 xenograft in nude mice.

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Involvement of NF-κB signaling pathway in the regulation of PRKAA1-mediated tumorigenesis in gastric cancer

Cited by 14 publications

References 49 publications

Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF‑κB signaling pathway

Inhibitory Effect of Hydroxysafflor Yellow Pigment A on Human Gastric Adenocarcinoma BGC-823 Xenograft in Nude Mice

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