Autophagy inhibition as a promising therapeutic target for laryngeal cancer

García-Mayea, Yoelsis; Mir, Cristina; Muñoz, Lisandra; Benavente, Sergio; Castellví, Josep; Temprana, Jordi; Maggio, Valentina; Lorente, Juan; Paciucci, Rosanna; Lleonart, Matilde E.

doi:10.1093/carcin/bgz080

Cited by 24 publications

(35 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of interest is that some of these markers had prognostic value when correlated with clinical variables (Figure 4). Besides, we suggested that the acquisition of resistance to cisplatin is related to the development of 5-fluorouracil resistance, supporting the presence of a common regulatory resistance pathway (187).…”

Section: Autophagy and Cancer Cell Resistancementioning

confidence: 55%

Autophagy Takes Center Stage as a Possible Cancer Hallmark

et al. 2020

Self Cite

View full text Add to dashboard Cite

Cancer remains one of the leading causes of death worldwide, despite significant advances in cancer research and improvements in anticancer therapies. One of the major obstacles to curing cancer is the difficulty of achieving the complete annihilation of resistant cancer cells. The resistance of cancer cells may not only be due to intrinsic factors or factors acquired during the evolution of the tumor but may also be caused by chemotherapeutic treatment failure. Conversely, autophagy is a conserved cellular process in which intracellular components, such as damaged organelles, aggregated or misfolded proteins and macromolecules, are degraded or recycled to maintain cellular homeostasis. Importantly, autophagy is an essential mechanism that plays a key role in tumor initiation and progression. Depending on the cellular context and microenvironmental conditions, autophagy acts as a double-edged sword, playing a role in inducing apoptosis or promoting cell survival. In this review, we propose several scenarios in which autophagy could contribute to cell survival or cell death. Moreover, a special focus on novel promising targets and therapeutic strategies based on autophagic resistant cells is presented.

show abstract

Section: Autophagy and Cancer Cell Resistancementioning

confidence: 55%

Autophagy Takes Center Stage as a Possible Cancer Hallmark

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…A stressful extracellular microenvironment, such as hypoxia or low glucose, may upregulate GLUT-1 expression [37]. Indeed, hypoxia promotes the proliferation, migration, and chemoresistance of CSCs [4][5][6][7]14,15]. In this study, the growth and migration of CD133 + Tu212 cells were greater than those of CD133 -Tu212 cells under hypoxic and low-glucose conditions; this was associated with increased mRNA and protein levels of GLUT-1 in CD133 + Tu212 cells.…”

Section: Discussionmentioning

confidence: 68%

“…CSCs are closely related to the occurrence, development, metastasis, recurrence, and chemoradiotherapy resistance of tumors [4]. Laryngeal CSCs reportedly express CD133 as a marker [5]. CD133 + CSCs have higher tumorigenic and invasive abilities than CD133cancer cells [5][6][7]10].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Inhibition of GLUT1 Expression and Autophagy Modulation on the Growth and Migration of Laryngeal Carcinoma Stem Cells under Hypoxic and Low-Glucose Conditions

Chen

Liu

Zhong

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Enhanced glucose uptake and autophagy are means by which cells adapt to stressful microenvironments. We investigated the roles of glucose transporter-1 (GLUT-1) and autophagy in laryngeal carcinoma stem cells under hypoxic and low-glucose conditions.Methods: CD133+ Tu212 laryngeal carcinoma stem cells were purified by magnetic-activated cell sorting and subjected to hypoxic and/or low-glucose conditions. Proliferation was evaluated using a cell-counting kit and a clone-formation assay, and migration was evaluated through a Transwell assay. Autophagy was assessed via transmission electron microscopy. GLUT-1 and beclin-1 expression were silenced using an shRNA and autophagy was manipulated using rapamycin, 3-MA, or chloroquine. Gene expression levels were evaluated by quantitative reverse transcription-polymerase chain reaction and protein concentrations were assessing via Western blotting.Results: Compared to CD133– stem cells, CD133+ cells showed increased proliferation and migration, and reduced apoptosis, under hypoxic or low-glucose conditions. They also showed increased expression of GLUT-1 and autophagy markers. Finally, GLUT-1 knockdown or autophagy inhibition reduced their proliferation and migration.Conclusions: Enhanced glucose uptake and autophagy maintain the functions of CD133+ laryngeal carcinoma stem cells under hypoxic and low-glucose conditions.

show abstract

Section: Introductionmentioning

confidence: 99%

Effect of Inhibition of GLUT1 Expression and Autophagy Modulation on the Growth and Migration of Laryngeal Carcinoma Stem Cells Under Hypoxic and Low-Glucose Conditions

Chen

Liu

Zhong

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Enhanced glucose uptake and autophagy are means by which cells adapt to stressful microenvironments. We investigated the roles of glucose transporter-1 (GLUT-1) and autophagy in laryngeal carcinoma stem cells under hypoxic and low-glucose conditions.Methods: CD133+ Tu212 laryngeal carcinoma stem cells were purified by magnetic-activated cell sorting and subjected to hypoxic and/or low-glucose conditions. Proliferation was evaluated using a cell-counting kit and a clone-formation assay, and migration was evaluated through a Transwell assay. Autophagy was assessed via transmission electron microscopy. GLUT-1 and beclin-1 expression were silenced using an shRNA and autophagy was manipulated using rapamycin, 3-MA, or chloroquine. Gene expression levels were evaluated by quantitative reverse transcription-polymerase chain reaction and protein concentrations were assessing via Western blotting. Results: Compared to CD133– stem cells, CD133+ cells showed increased proliferation and migration, and reduced apoptosis, under hypoxic or low-glucose conditions. They also showed increased expression of GLUT-1 and autophagy markers. Finally, GLUT-1 knockdown or autophagy inhibition reduced their proliferation and migration.Conclusions: Enhanced glucose uptake and autophagy maintain the functions of CD133+ laryngeal carcinoma stem cells under hypoxic and low-glucose conditions.

show abstract

Autophagy inhibition as a promising therapeutic target for laryngeal cancer

Cited by 24 publications

References 40 publications

Autophagy Takes Center Stage as a Possible Cancer Hallmark

Autophagy Takes Center Stage as a Possible Cancer Hallmark

Effect of Inhibition of GLUT1 Expression and Autophagy Modulation on the Growth and Migration of Laryngeal Carcinoma Stem Cells under Hypoxic and Low-Glucose Conditions

Effect of Inhibition of GLUT1 Expression and Autophagy Modulation on the Growth and Migration of Laryngeal Carcinoma Stem Cells Under Hypoxic and Low-Glucose Conditions

Contact Info

Product

Resources

About