c-Jun NH&lt;sub&gt;2&lt;/sub&gt;-terminal kinase (JNK)/stress-activated protein kinase-associated protein 1 (JSAP1) attenuates curcumin-induced cell death differently from its family member, JNK-associated leucine zipper protein (JLP)

Gunarta, I Ketut; Yuliana, Dewi; Erdenebaatar, Purev; Kishi, Yuhei; Boldbaatar, Jambaldorj; Suzuki, Ryusuke; Odongoo, Ravdandorj; Davaakhuu, Gantulga; Hohjoh, Hirohiko; Yoshioka, Katsuji

doi:10.5582/ddt.2021.01021

Cited by 3 publications

(2 citation statements)

References 36 publications

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“…HCT116 cells either expressing or not expressing Oryza sativa transport inhibitor response 1 (OsTIR1) (F74G) were cultured as previously described (21,22). In some experiments, HCT116 cells were synchronized at the G1/S boundary, as described by Boulay et al (23), with minor modifications.…”

Section: Cell Culture and Reagentsmentioning

confidence: 99%

Redundant roles of extra-cellular signal-regulated kinase (ERK) 1 and 2 in the G1-S transition and etoposide-induced G2/M checkpoint in HCT116 cells

Erdenebaatar

Gunarta

Suzuki

et al. 2023

DD&T

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Cell cycle, DNA damage, mitogen-activated protein kinaseThe extracellular signal-regulated kinase (ERK) 1 and 2 intracellular signaling pathways play key roles in a variety of cellular processes, such as proliferation and differentiation. Dysregulation of ERK1/2 signaling has been implicated in many diseases, including cancer. Although ERK1/2 signaling pathways have been extensively studied, controversy remains as to whether ERK1 and ERK2 have specific or redundant functions. In this study, we examined the functional roles of ERK1 and ERK2 in cell proliferation and cell cycle progression using an auxin-inducible degron system combined with gene knockout technology. We found that ERK1/2 double depletion, but not ERK1 or ERK2 depletion, substantially inhibited the proliferation of HCT116 cells during G1-S transition. We further demonstrated that ERK1/2-double-depleted cells were much more tolerant to etoposide-induced G2/M arrest than ERK1 or ERK2 single-knockout cells. Together, these results strongly suggest the functional redundancy of ERK1 and ERK2 in both the G1-S transition under physiological conditions and the DNA damage-induced G2/M checkpoint. Our findings substantially advance understanding of the ERK1/2 pathways, which could have strong implications for future pharmacological developments.

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Section: Cell Culture and Reagentsmentioning

confidence: 99%

Redundant roles of extra-cellular signal-regulated kinase (ERK) 1 and 2 in the G1-S transition and etoposide-induced G2/M checkpoint in HCT116 cells

Erdenebaatar

Gunarta

Suzuki

et al. 2023

DD&T

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“…In human colon carcinoma cells (HCT-116 cells), curcumin-mediated cytotoxicity was attenuated by the expression of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase associated protein 1 (JSAP1), a scaffold protein involved in JNK signaling pathway and lysosomal transport with an increase in autophagy. Knockout of JSAP1 attenuated autophagic flux and sensitised the cells towards curcumin treatment [ 132 ]. Curcumin treatment in colorectal cancer cells evoked pro-survival autophagy via cathepsin C, the lysosomal acid hydrolase, to offer chemotherapeutic resistance in cancer cells.…”

Section: Roles Of Polyphenols In Autophagic Adaptation For Healthy Agingmentioning

confidence: 99%

Plant Polyphenols for Aging Health: Implication from Their Autophagy Modulating Properties in Age-Associated Diseases

et al. 2021

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Polyphenols are a family of naturally occurring organic compounds, majorly present in fruits, vegetables, and cereals, characterised by multiple phenol units, including flavonoids, tannic acid, and ellagitannin. Some well-known polyphenols include resveratrol, quercetin, curcumin, epigallocatechin gallate, catechin, hesperetin, cyanidin, procyanidin, caffeic acid, and genistein. They can modulate different pathways inside the host, thereby inducing various health benefits. Autophagy is a conserved process that maintains cellular homeostasis by clearing the damaged cellular components and balancing cellular survival and overall health. Polyphenols could maintain autophagic equilibrium, thereby providing various health benefits in mediating neuroprotection and exhibiting anticancer and antidiabetic properties. They could limit brain damage by dismantling misfolded proteins and dysfunctional mitochondria, thereby activating autophagy and eliciting neuroprotection. An anticarcinogenic mechanism is stimulated by modulating canonical and non-canonical signalling pathways. Polyphenols could also decrease insulin resistance and inhibit loss of pancreatic islet β-cell mass and function from inducing antidiabetic activity. Polyphenols are usually included in the diet and may not cause significant side effects that could be effectively used to prevent and treat major diseases and ailments.

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Small heterodimer partner interacting leucine zipper protein (SMILE) ameliorates autoimmune arthritis via AMPK signaling pathway and the regulation of B cell activation

et al. 2023

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Rheumatoid arthritis (RA) is an autoimmune disease that causes joint swelling and inflammation and can involve the entire body. RA is characterized by the increase of pro-inflammatory cytokines such as interleukin (IL) and tumor necrosis factor, and the over-activation of T lymphocytes and B lymphocytes, which may lead to severe chronic inflammation of joints. However, despite numerous studies the pathogenesis and treatment of RA remain unresolved. This study investigated the use of small heterodimer partner-interacting leucine zipper protein (SMILE) overexpression to treat a mouse model of RA. SMILE is an insulin-inducible corepressor through adenosine monophosphate-activated kinase (AMPK) signaling pathway. The injection of a SMILE overexpression vector to mice with collagen induced-arthritis resulted in a milder clinical pathology and a reduced incidence of arthritis, less joint tissue damage, and lower levels of Th17 cells and plasma B cells in the spleen. Immunohistochemistry of the joint tissue showed that SMILE decreased B-cell activating factor (BAFF) receptor (BAFF-R), mTOR, and STAT3 expression but increased AMPK expression. In SMILE-overexpressing transgenic mice with collagen antibody-induced arthritis (CAIA), a decrease in the arthritis score and reductions in tissue damage, the number of B cells, and antibody production were observed. The treatment of immune cells in vitro with curcumin, a known SMILE-inducing agent, led to decreases in plasma B cells, germinal center B cells, IL-17-producing B cells, and BAFF-R-positive B cells. Taken together, our findings demonstrate the therapeutic potential of SMILE in RA, based on its inhibition of B cell activation mediated by the AMPK/mTOR and STAT3 signaling pathway and BAFF-R expression.

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c-Jun NH<sub>2</sub>-terminal kinase (JNK)/stress-activated protein kinase-associated protein 1 (JSAP1) attenuates curcumin-induced cell death differently from its family member, JNK-associated leucine zipper protein (JLP)

Cited by 3 publications

References 36 publications

Redundant roles of extra-cellular signal-regulated kinase (ERK) 1 and 2 in the G1-S transition and etoposide-induced G2/M checkpoint in HCT116 cells

Redundant roles of extra-cellular signal-regulated kinase (ERK) 1 and 2 in the G1-S transition and etoposide-induced G2/M checkpoint in HCT116 cells

Plant Polyphenols for Aging Health: Implication from Their Autophagy Modulating Properties in Age-Associated Diseases

Small heterodimer partner interacting leucine zipper protein (SMILE) ameliorates autoimmune arthritis via AMPK signaling pathway and the regulation of B cell activation

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