Role of PI3K/Akt/mTOR and MEK/ERK pathway in Concanavalin A induced autophagy in HeLa cells

Roy, Bibhas; Pattanaik, Arup K.; Das, Jayeeta; Bhutia, Sujit K.; Behera, Birendra; Singh, Prashant; Maiti, Tapas K.

doi:10.1016/j.cbi.2014.01.003

Cited by 97 publications

(69 citation statements)

References 34 publications

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“…The PI3K/Akt/Raptor-mTOR (mTORC1) signaling pathway is a well characterized signaling cascade, which is involved in the regulation of autophagy (19,20). The Akt/mTOR signaling pathway in particular has a significant role in the regulation of autophagy (21,22). For these reasons, whether PM 2.5 regulated autophagy via activation of Akt/mTOR signaling was evaluated.…”

Section: Pm 2 5 Induces the Expression Of Morphological And Biochemimentioning

confidence: 99%

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

Wang

et al. 2015

Molecular Medicine Reports

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Abstract. Particulate matter 2.5 (PM 2.5 ) is a significant risk factor for asthma. A recent study revealed that autophagy was associated with asthma pathogenesis. However, the specific mechanisms underlying PM 2.5 -induced autophagy in asthma have remained elusive. In the present study, PM 2.5 -induced autophagy was evaluated in Beas-2B human bronchial epithelial cells and the potential molecular mechanisms were investigated. Using electron microscopy, immunofluorescence staining and immunoblot studies, it was confirmed that PM 2.5 induced autophagy in Beas-2B cells as a result of PM 2.5 -mediated inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway in Beas-2B cells. LY294002, a PI3K inhibitor, reduced the accumulation of microtubule-associated protein 1 light chain 3 II and attenuated the effect of PM 2.5 . Phosphorylated (p-)p38, p-extracellular signal-regulated kinase and p-c-Jun N-terminal kinase were dephosphorylated following exposure to PM 2.5 . The roles of p53, reactive oxygen species scavenger tetramethylthiourea and autophagy inhibitor 3-methyladenine in PM 2.5 -induced autophagy in Beas-2B cells were also investigated. The results suggested that the PI3K/Akt/mTOR signaling pathway may be a key contributor to PM 2.5 -induced autophagy in Beas-2B cells. The results of the present study therefore provided an a insight into potential future clinical applications targeting these signaling pathways, for the prevention and/or treatment of PM 2.5 -induced lung diseases. IntroductionAcute and chronic exposure to particulate matter (PM), particularly fine particles with aerodynamic diameters of ≤2.5 µm PM 2.5 , has been shown to increase the number of hospital admissions for respiratory causes amongst the general population (1). Evidence obtained from environmental and epidemiological studies has revealed a marked association between fine particulate air pollution and multiple health issues, including respiratory illnesses (for example, respiratory track inflammation, asthma, acute bronchitis and lung cancer) as well as cardiovascular disease mortality (2-4).Increasing evidence supporting a link between traffic-associated air pollution and the incidence of childhood asthma has emerged; however, published estimates highlight the variability observed between populations (5,6). Asthma is a common worldwide respiratory symptom complex, frequently involving airway inflammation, which results in clinically significant physiological airway dysfunction. Asthma pathogenesis is complex, and multiple factors have roles in the development of the disease (7).Autophagy describes an evolutionarily conserved and tightly regulated lysosomal pathway, responsible for the degradation of macromolecules, including proteins, glycogen, lipids, nucleotides and organelles, via several complex pathways (8).Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial ...

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Section: Pm 2 5 Induces the Expression Of Morphological And Biochemimentioning

confidence: 99%

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

Wang

et al. 2015

Molecular Medicine Reports

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“…Activated Akt can make Ser939 sites and THrl462 sites phosphorylated on TSC-2. And then indirectly or directly activate mTOR, promoting the invasion of various tumor cells, including cervical cancer cells [3,4]. mTOR is an atypical serine/threonine protein kinase comprised by more than 2000 amino acids, which can make threonine phosphorylation and is also one member of PI3K family.…”

Section: Discussionmentioning

confidence: 99%

“…mTOR is an atypical serine/threonine protein kinase comprised by more than 2000 amino acids, which can make threonine phosphorylation and is also one member of PI3K family. Akt/ mTOR signaling pathway activation is closely related with development of metastasis in breast cancer [17], melanoma [18,19], pancreatic cancer [20,21], cervical cancer [3,4]. In up to 95% of cervical cancer tissue, there is mTOR signaling pathway activation which plays an important role in the development of cervical cancer [22].…”

Section: Discussionmentioning

confidence: 99%

“…As same as the majority of cancer, with poor prevention and treatment effects and more complex pathogenesis, cervical cancer is affected by many cell signaling pathways [2]. And the invasion and metastasis of cervical cancer is related with Akt/mTOR signaling pathway closely [3,4] . Matrix metalloproteinase (MMP) 2 and MMP 9 are the downstream targets in Akt/mTOR signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

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Effect of bortezomib on migration and invasion in cervical carcinoma HeLa cell

Shi¹,

Zhang

Yin

2015

Asian Pacific Journal of Tropical Medicine

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“…An evidence indicated that SMI-4a could promote apoptosis in vitro. The complex interplay between PI3K/AKT/mTOR axis and the autophagic process is well documented [15][16][17]. The PI3K/Akt/mTOR signaling pathway negatively regulates autophagy through phosphorylation of Akt, downstream effector mTOR, and its substrate p70S6K [18].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy enhances SMI-4a-induced growth inhibition and apoptosis of melanoma cells

Chen¹,

Lv²,

Liu³

et al. 2018

Trop. J. Pharm Res

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Purpose: To investigate the exact role of the proviral integration site for Moloney murine leukemia virus-1 (PIM-1) on autophagy as well as the underlying molecular mechanisms in melanoma. Methods: mRNA expression levels in A375 and G361 human melanoma cell lines were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Enzyme-linked immunosorbent (ELISA) and western blotting assays were applied to determine protein expression levels, while cell viability was evaluated using Cell Counting Kit 8 and colony formation assay. Flow cytometric analysis and caspase 3/7 activity assay were used to assess apoptosis. Results: The results show that pharmacological inhibition of PIM-1 with its potent inhibitor (SMI-4a) suppressed cell viability and induced apoptosis in melanoma cell lines A375 and G361. SMI-4a also induced autophagy through inhibition of the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) axis in melanoma cells

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Role of PI3K/Akt/mTOR and MEK/ERK pathway in Concanavalin A induced autophagy in HeLa cells

Cited by 97 publications

References 34 publications

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

Effect of bortezomib on migration and invasion in cervical carcinoma HeLa cell

Inhibition of autophagy enhances SMI-4a-induced growth inhibition and apoptosis of melanoma cells

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