Expression and role of p16 and <scp>GLUT1</scp> in malignant diseases and lung cancer: A review

Pezzuto, Aldo; D’Ascanio, Michela; Rícci, Alberto; Pagliuca, Alessandra; Carico, Elisabetta

doi:10.1111/1759-7714.13651

Cited by 43 publications

(37 citation statements)

References 96 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Glycolysis not only provides energy for cancer cells but also produces important metabolic intermediates, which exert crucial roles in maintaining cell proliferation, migration, and invasion. 16 , 17 HK2 is a speed-limiting enzyme in the glycolysis process. 18 LDHA, an important HIF-1α target, can catalyze the reduction of pyruvate to lactate and maintain cell survival under hypoxic conditions.…”

Section: Discussionmentioning

confidence: 99%

Circ_0001944 Contributes to Glycolysis and Tumor Growth by Upregulating NFAT5 Through Acting as a Decoy for miR-142-5p in Non-Small Cell Lung Cancer

Dou¹,

Tian²,

Wang³

et al. 2021

CMAR

View full text Add to dashboard Cite

Background: Circular RNAs (circRNAs) participate in the tumorigenesis of various cancers. CircRNA hsa_circ_0001944 (circ_0001944), derived from the TCONS_l2_00030860 gene, has been uncovered to be upregulated in NSCLC (non-small cell lung cancer). Nevertheless, the influence of circ_0001944 on glycolysis and tumor growth in NSCLC is unclear. Methods: Expression trend of circ_0001944 in NSCLC tissues and cells were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Loss-of-function experiments were performed to assess the influence of circ_0001944 knockdown on proliferation, migration, invasion, and glycolysis of NSCLC cells. Protein levels were assessed by Western blotting. The regulatory mechanism of circ_0001944 was analyzed by bioinformatics analysis, dual-luciferase reporter assay, and/or RNA pull-down assay. The tumorigenicity of circ_0001944 was confirmed by xenograft assay. Results: Circ_0001944 was highly expressed in NSCLC, and NSCLC patients with high expression of circ_0001944 had a worse prognosis. Circ_0001944 silencing decreased xenograft tumor growth in vivo and repressed proliferation, migration, invasion, and glycolysis of NSCLC cells in vitro. Circ_0001944 was verified as a decoy for microRNA (miR)-142-5p, which targeted NFAT5 (nuclear factor of activated T cells 5). MiR-142-5p was downregulated while NFAT5 was upregulated in NSCLC. Both miR-142-5p inhibition and NFAT5 overexpression offset the suppressive impact of circ_0001944 silencing on proliferation, migration, invasion, and glycolysis of NSCLC cells. Circ_0001944 adsorbed miR-142-5p to elevate NFAT5 expression in NSCLC cells. Conclusion: Circ_0001944 promotes proliferation, migration, invasion, and glycolysis of NSCLC cells by upregulating NFAT5 through adsorbing miR-142-5p, offering a novel mechanism for understanding the advancement of NSCLC.

show abstract

Section: Discussionmentioning

confidence: 99%

Circ_0001944 Contributes to Glycolysis and Tumor Growth by Upregulating NFAT5 Through Acting as a Decoy for miR-142-5p in Non-Small Cell Lung Cancer

Dou¹,

Tian²,

Wang³

et al. 2021

CMAR

View full text Add to dashboard Cite

show abstract

“…Several types of research have pointed out the role played by galectin-3 in cell cycle and cell death, whose interplay is of great importance both in carcinogenesis and chemotherapy. The tumor suppressor proteins playing a key role in cell cycle regulation such as p16 [113] are reported to be networking with galectin expression and signaling pathway. p16 has been reported to decrease mRNA stability and thereby down-regulating its galectin-3 expression level in the cell [114].…”

Section: Galectin-3 In Modulating Tumor Development and Sustaining The Proliferative Potentialmentioning

confidence: 99%

Galectin-3: A factotum in carcinogenesis bestowing an archery for prevention

Ram

Lekshmi

Somanathan

et al. 2021

TUB

View full text Add to dashboard Cite

Cancer metastasis and therapy resistance are the foremost hurdles in oncology at the moment. This review aims to pinpoint the functional aspects of a unique multifaceted glycosylated molecule in both intracellular and extracellular compartments of a cell namely galectin-3 along with its metastatic potential in different types of cancer. All materials reviewed here were collected through the search engines PubMed, Scopus, and Google scholar. Among the 15 galectins identified, the chimeric gal-3 plays an indispensable role in the differentiation, transformation, and multi-step process of tumor metastasis. It has been implicated in the molecular mechanisms that allow the cancer cells to survive in the intravascular milieu and promote tumor cell extravasation, ultimately leading to metastasis. Gal-3 has also been found to have a pivotal role in immune surveillance and pro-angiogenesis and several studies have pointed out the importance of gal-3 in establishing a resistant phenotype, particularly through the epithelial-mesenchymal transition process. Additionally, some recent findings suggest the use of gal-3 inhibitors in overcoming therapeutic resistance. All these reports suggest that the deregulation of these specific lectins at the cellular level could inhibit cancer progression and metastasis. A more systematic study of glycosylation in clinical samples along with the development of selective gal-3 antagonists inhibiting the activity of these molecules at the cellular level offers an innovative strategy for primary cancer prevention.

show abstract

“…In contrast, propofol downregulated GLUT1, which resulted in the less uptake of glucose from media, and hence the concentration of glucose was increased after propofol exposure. The cellular glucose uptakevia high level of GLUT1 expression was correlated with the malignancy of cancers (Leung, 2004;Pezzuto et al, 2020) and the overexpression of GLUT1 in cancer cells were essential for the high rate of glycolysis (Wright, 2020). Propofol was reported to downregulateGLUT1 gene in macrophages (Tanaka et al, 2010) and this was in line with the downregulation of GLUT1 proteins in the rat brain tissue under hypoxic preconditioning (Xiao et al, 2020).…”

Section: Discussionmentioning

confidence: 94%

“…Glucose is taken up by cancer cells through glucose transporter 1 (GLUT1) and transformed to pyruvate, which is converted to lactate rather than enters mitochondria via mitochondrial pyruvate carrier 1 (MPC1) to be utilised by TCA cycle (Pezzuto, D'Ascanio, Ricci, Pagliuca, & Carico, 2020;Zou et al, 2019). Glutamine can be transformed to be glutamate under the catalysation of glutamate dehydrogenase 1 (GLUD1) for using in the TCA cycle which generates crucial intermediates for cancer growth and survival (Craze et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane but not propofol enhances ovarian cancer cell malignancy through regulating cellular metabolic and signalling mechanisms

Wang

Liu

et al. 2021

Preprint

View full text Add to dashboard Cite

Background and Purpose: Surgery remains the first-line treatment of ovarian cancer. However, perioperative risk factors including the choice of anaesthetics may influence its recurrence after surgery. In the current study, it was hypothesised that inhalational anaesthetic sevoflurane and intravenous anaesthetic propofol might affect cancer cellular metabolism and signalling, which might interfere the malignancy of ovarian cancer cells. Experimental Approach: Cultured ovarian cancer cells were exposed to 2.5% sevoflurane or administered with 4 μg/mL propofol for 2 hours followed by 24 hours recovery. Their cell viability, proliferation, migration and invasion were assessed using cell counting kit-8, Ki-67 staining, wound healing and Transwell assay. Cellular signalling biomarkers were measured using immunofluorescent staining and/or Western blot. Cultured media were collected for 1H-NMR spectroscopy-based metabolomics analysis. Key Results: The cell viability, proliferation, migration, and invasion of ovarian cancer cells were enhanced by sevoflurane but suppressed by propofol. Sevoflurane increased the GLUT1, MPC1, GLUD1, p-Erk1/2, and HIF-1α expressions but decreased the PEDF expression. In contrast to the sevoflurane treatment, the “mirror changes” of these cellular markers were observed with propofol. Sevoflurane increased levels of isopropanol but decreased glucose and glutamine levels in the media, but the opposite changes of those metabolites were found after propofol treatment. Conclusion and Implications: These data indicated that unlike propofol, sevoflurane enhanced ovarian cancer cell metabolism and activated PEDF/Erk/HIF-1α cellular signalling pathway, suggesting that sevoflurane might have pro-tumour property but propofol might afford an anti-tumour property. The translational value of this work warrants further study.

show abstract

Expression and role of p16 and GLUT1 in malignant diseases and lung cancer: A review

Cited by 43 publications

References 96 publications

Circ_0001944 Contributes to Glycolysis and Tumor Growth by Upregulating NFAT5 Through Acting as a Decoy for miR-142-5p in Non-Small Cell Lung Cancer

Circ_0001944 Contributes to Glycolysis and Tumor Growth by Upregulating NFAT5 Through Acting as a Decoy for miR-142-5p in Non-Small Cell Lung Cancer

Galectin-3: A factotum in carcinogenesis bestowing an archery for prevention

Sevoflurane but not propofol enhances ovarian cancer cell malignancy through regulating cellular metabolic and signalling mechanisms

Contact Info

Product

Resources

About