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Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE227641 | GEO | 2023/03/22

REPOSITORIES: GEO

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Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq I]

Project description:To investigate if CRC cells treated with CoCl2, brefeldin A, or low glucose for more than 30 days exhibited an increased senescence.

2023-03-22 | GSE227379 | GEO

Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq II]

Project description:To investigate if oxaliplatin resistance contributed to persistent endoplasmic reticulum-induced senescence,

2023-03-22 | GSE227609 | GEO

Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer

Project description:Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer

| PRJNA946144 | ENA

Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq I]

Project description:Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq I]

| PRJNA944924 | ENA

Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq II]

Project description:Inositol hexaphosphate enhances chemotherapy by reversing persistent endoplasmic reticulum stress-induced senescence in colorectal cancer [RNA-seq II]

| PRJNA945902 | ENA

Inositol Requiring Enzyme (IRE), a multiplayer in sensing endoplasmic reticulum stress.

Project description:The endoplasmic reticulum (ER) can sense a wide variety of external and internal perturbations and responds by mounting stress coping responses, such as the unfolded protein response (UPR). The UPR is composed of three stress sensors, namely IRE1α, PERK, and ATF6 that are activated to re-establish ER homeostasis. IRE1α represents the most ancient branch of the UPR affecting many cellular processes in plant and animal cells. IRE1α is a type I transmembrane protein with kinase/nuclease activities in response to ER stress. Both the ER luminal and cytosolic IRE1α interactomes have been identified revealing a multifunctional role of the ER stress sensor. IRE1α is also associated with organellar membrane contacts to promote rapid communication between intracellular organelles under stress conditions.

| S-EPMC8765250 | biostudies-literature

Endoplasmic reticulum stress enhances fibrotic remodeling in the lungs.

Project description:Evidence of endoplasmic reticulum (ER) stress has been found in lungs of patients with familial and sporadic idiopathic pulmonary fibrosis. We tested whether ER stress causes or exacerbates lung fibrosis by (i) conditional expression of a mutant form of surfactant protein C (L188Q SFTPC) found in familial interstitial pneumonia and (ii) intratracheal treatment with the protein misfolding agent tunicamycin. We developed transgenic mice expressing L188Q SFTPC exclusively in type II alveolar epithelium by using the Tet-On system. Expression of L188Q SFTPC induced ER stress, as determined by increased expression of heavy-chain Ig binding protein (BiP) and splicing of X-box binding protein 1 (XBP1) mRNA, but no lung fibrosis was identified in the absence of a second profibrotic stimulus. After intratracheal bleomycin, L188Q SFTPC-expressing mice developed exaggerated lung fibrosis and reduced static lung compliance compared with controls. Bleomycin-treated L188Q SFTPC mice also demonstrated increased apoptosis of alveolar epithelial cells and greater numbers of fibroblasts in the lungs. With a complementary model, intratracheal tunicamycin treatment failed to induce lung remodeling yet resulted in augmentation of bleomycin-induced fibrosis. These data support the concept that ER stress produces a dysfunctional epithelial cell phenotype that facilitates fibrotic remodeling. ER stress pathways may serve as important therapeutic targets in idiopathic pulmonary fibrosis.

| S-EPMC3127925 | biostudies-literature

Photothermal Therapy <i>via</i> NIR II Light Irradiation Enhances DNA Damage and Endoplasmic Reticulum Stress for Efficient Chemotherapy.

Project description:Ovarian cancer has the highest death rate in gynecologic tumors and the main therapy for patients with advanced is chemotherapy based on cisplatin. Additionally, hyperthermic intraperitoneal has been used in clinic to obtain better efficacy for patients. Hence, combined photothermal therapy with platinum drugs in a new delivery system might bring new hope for ovarian cancer. A reduction sensitive polymer encapsulating a Pt (IV) prodrug and a near infrared II (NIR II) photothermal agent IR1048 to form nanoparticles were reported to enhance the efficacy of ovarian cancer treatment. At the same time, endoplasmic reticulum stress indicates an imbalance in proteostasis which probably caused by extrinsic stress such as chemotherapy and the temperature changed. The efficacy of nanoparticles containing Pt (IV) and IR1048 under NIR II light might be caused via increased DNA damage and endoplasmic reticulum (ER) stress.

| S-EPMC8117088 | biostudies-literature

Celecoxib enhances radiosensitivity of hypoxic glioblastoma cells through endoplasmic reticulum stress.

Project description:BackgroundRefractoriness of glioblastoma multiforme (GBM) largely depends on its radioresistance. We investigated the radiosensitizing effects of celecoxib on GBM cell lines under both normoxic and hypoxic conditions.MethodsTwo human GBM cell lines, U87MG and U251MG, and a mouse GBM cell line, GL261, were treated with celecoxib or γ-irradiation either alone or in combination under normoxic and hypoxic conditions. Radiosensitizing effects were analyzed by clonogenic survival assays and cell growth assays and by assessing apoptosis and autophagy. Expression of apoptosis-, autophagy-, and endoplasmic reticulum (ER) stress-related genes was analyzed by immunoblotting.ResultsCelecoxib significantly enhanced the radiosensitivity of GBM cells under both normoxic and hypoxic conditions. In addition, combined treatment with celecoxib and γ-irradiation induced marked autophagy, particularly in hypoxic cells. The mechanism underlying the radiosensitizing effect of celecoxib was determined to be ER stress loading on GBM cells.ConclusionCelecoxib enhances the radiosensitivity of GBM cells by a mechanism that is different from cyclooxygenase-2 inhibition. Our results indicate that celecoxib may be a promising radiosensitizing drug for clinical use in patients with GBM.

| S-EPMC3748914 | biostudies-literature

Endoplasmic Reticulum Stress Enhances Mitochondrial Metabolic Activity in Mammalian Adrenals and Gonads.

Project description:The acute response to stress consists of a series of physiological programs to promote survival by generating glucocorticoids and activating stress response genes that increase the synthesis of many chaperone proteins specific to individual organelles. In the endoplasmic reticulum (ER), short-term stress triggers activation of the unfolded protein response (UPR) module that either leads to neutralization of the initial stress or adaptation to it; chronic stress favors cell death. UPR induces expression of the transcription factor, C/EBP homology protein (CHOP), and its deletion protects against the lethal consequences of prolonged UPR. Here, we show that stress-induced CHOP expression coincides with increased metabolic activity. During stress, the ER and mitochondria come close to each other, resulting in the formation of a complex consisting of the mitochondrial translocase, translocase of outer mitochondrial membrane 22 (Tom22), steroidogenic acute regulatory protein (StAR), and 3?-hydroxysteroid dehydrogenase type 2 (3?HSD2) via its intermembrane space (IMS)-exposed charged unstructured loop region. Stress increased the circulation of phosphates, which elevated pregnenolone synthesis by 2-fold by increasing the stability of 3?HSD2 and its association with the mitochondrion-associated ER membrane (MAM) and mitochondrial proteins. In summary, cytoplasmic CHOP plays a central role in coordinating the interaction of MAM proteins with the outer mitochondrial membrane translocase, Tom22, to activate metabolic activity in the IMS by enhanced phosphate circulation.

| S-EPMC5126293 | biostudies-literature

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