Deletion of etoposide-induced 2.4 kb transcript (ei24) reduced cell proliferation and aggregate-size in Dictyostelium discoideum

Gupta, Neha; Saran, Shweta

doi:10.1387/ijdb.170327ss

Cited by 7 publications

(8 citation statements)

References 25 publications

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“…They suggested that EI24 acts as a tumor suppressor in skin cancer. Additionally, it has been reported that EI24 is involved in the survival and growth of non-tumor cells such as pancreatic β-cells and Dictyostelium discoideum (21, 22). EI24 has been reported as a tumor suppressor even in pancreatic cancer cells, which is in conflict with our observations (23).…”

Section: Discussionmentioning

confidence: 99%

EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation

et al. 2019

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Autophagy is a highly conserved cellular process in which cytoplasmic materials are degraded and recycled as energy sources when nutrient supplies are lacking. Established tumor cells require autophagy for cell growth and tumor promotion. In particular, the survival of pancreatic tumor cells appears to be strongly dependent on autophagy, referred to as autophagy addiction. This dependency of pancreatic tumor cells on autophagy may be a candidate target for pancreatic tumor therapy. EI24 (etoposide-induced gene 2.4 kb; PIG8, p53-induced gene 8) acts as a tumor suppressor, inhibiting cell growth and inducing apoptosis in breast, cervical, and prostate cancer cells. However, recent papers have reported that EI24 is an essential component of the autophagy pathway. This newly discovered role of EI24 as a component of autophagy may act as a tumor promoter, which is contradictory to its known role as a tumor suppressor. We investigated the role of EI24 as a component of autophagy in pancreatic tumor cell proliferation. Here, we demonstrated that knockdown of EI24 using siRNA in pancreatic tumor cells led to impaired autophagy at a late step (increase in LC3-II and accumulation of p62 and autolysosomes). EI24 deficiency in pancreatic tumor cell lines inhibited cell proliferation. We confirmed that loss of EI24 inhibited pancreatic cell proliferation using the CRISPR-Cas9 system. However, loss of EI24 in other cell lines did not affect cell proliferation. Taken together, our results suggest that EI24 acts as a tumor promoter in pancreatic tumor cells, and studying the role of EI24 in reference to its cellular context may lead to a useful therapeutic target.

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Section: Discussionmentioning

confidence: 99%

EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation

et al. 2019

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“…The absorbance was read at 405 nm. All measurements were normalized to protein concentrations determined by Bradford assay 11 …”

Section: Methodsmentioning

confidence: 99%

“…All measurements were normalized to protein concentrations determined by Bradford assay. 11 2.9 | Reactive oxygen species (ROS) levels 6×10 6 cells/ml were incubated with 30 μM Dihydroethidium (D7008; Sigma-Aldrich) for 30 min in the dark, washed twice in chilled KK2 buffer and immediately processed for flow-cytometer (BD-FACSAria Fusion). 12…”

Section: Camp Levelsmentioning

confidence: 99%

Metabolic signals influence cell‐fate decisions in Dictyostelium discoideum

Fatima,

Hadem,

Saran

2023

Cell Biochemistry & Function

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Nutrient‐sensing plays a crucial role in maintaining cellular energy and metabolic homeostasis. Perturbations in sensing pathways are associated with a wide variety of pathologies, especially metabolic diseases. Very little is understood about sensing fluctuations in nutrients and how this information is integrated into physiological and metabolic adaptation that could further affect cell‐fate decisions during differentiation in Dictyostelium discoideum (henceafter, Dictyostelium). Glucose is the primary metabolic fuel among all nutrients. Carbohydrates, lipids and proteins ultimately breakdown into glucose, which is further used for providing energy. The maintenance of optimum glucose levels is important for efficient cell‐survival. Glucose is not only a nutrient, but also a signaling molecule influencing cell growth and differentiation in Dictyostelium. Modulation of endogenous glucose levels either by varying exogenous glucose levels or genetic overexpression or deletion of genes involved in glucose signaling lead to changes in endogenous metabolite levels such as ADP/ATP ratio, NAD+/NADH ratio, cAMP and ROS levels which further influence cell‐fate decisions. Here, we show that AMPKα and Sir2D are components of glucose‐signaling pathway in Dictyostelium which adjust cell metabolism interdependently in response to nutrient‐status and promote cell‐fate decisions.

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“…For the first time, they showed that apart from being an energy sensor, AMPK also has a role in aggregate-size determination and cell patterning (Maurya et al, 2018). Saran's interest in the etoposide-induced 2.4 kb transcript (ei24) gene that is induced both by p53 and etoposide, an anti-cancer tumour drug allowed to understand its role in D. discoideum which does not possess a p53 protein (Gupta and Saran, 2018). Their work shows that EI24 (an autophagy associated transmembrane protein) is a key protein involved in autophagy (Gupta and Saran, 2019).…”

Section: Developmental Cell Deathmentioning

confidence: 99%

Glimpses of Dictyostelid research in India

Begum¹,

Saran²

2020

Int. J. Dev. Biol.

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Simple organisms are preferred for understanding the molecular and cellular function(s) of complex processes. Dictyostelium discoideum is a lower eukaryote, a protist and a cellular slime mould, which has been in recent times used for various studies such as cell differentiation, development, cell death, stress responses etc. It is a soil amoeba (unicellular) that undertakes a remarkable, facultative shift to multicellularity when exposed to starvation and requires signal pathways that result in alteration of gene expression and finally show cell differentiation. The amoebae aggregate, differentiate and form fruiting bodies with two terminally differentiated cells: the dead stalk (non-viable) and dormant spores (viable). In India, starting from the isolation of Dictyostelium species to morphogenesis, cell signalling and social evolution has been studied with many more new research additions. Advances in molecular genetics make Dictyostelium an attractive model system to study cell biology, biochemistry, signal transduction and many more.

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Deletion of etoposide-induced 2.4 kb transcript (ei24) reduced cell proliferation and aggregate-size in Dictyostelium discoideum

Cited by 7 publications

References 25 publications

EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation

EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation

Metabolic signals influence cell‐fate decisions in Dictyostelium discoideum

Glimpses of Dictyostelid research in India

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