Targeting Ca2+ signaling: A new arsenal against cancer

Panda, Suman; Chatterjee, Oishika; Roy, Laboni; Chatterjee, Subhrangsu

doi:10.1016/j.drudis.2021.11.012

Cited by 17 publications

(11 citation statements)

References 116 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dysregulation of Ca 2+ signaling and altered levels of intracellular Ca 2+ are involved in a plethora of processes in carcinogenesis, progression and chemoresistance of multiple cancer cell types [170]. Mounting evidence has…”

Section: Ca 2+ Signalingmentioning

confidence: 99%

Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer

et al. 2022

View full text Add to dashboard Cite

Exosomes are well-known key mediators of intercellular communication and contribute to various physiological and pathological processes. Their biogenesis involves four key steps, including cargo sorting, MVB formation and maturation, transport of MVBs, and MVB fusion with the plasma membrane. Each process is modulated through the competition or coordination of multiple mechanisms, whereby diverse repertoires of molecular cargos are sorted into distinct subpopulations of exosomes, resulting in the high heterogeneity of exosomes. Intriguingly, cancer cells exploit various strategies, such as aberrant gene expression, posttranslational modifications, and altered signaling pathways, to regulate the biogenesis, composition, and eventually functions of exosomes to promote cancer progression. Therefore, exosome biogenesis-targeted therapy is being actively explored. In this review, we systematically summarize recent progress in understanding the machinery of exosome biogenesis and how it is regulated in the context of cancer. In particular, we highlight pharmacological targeting of exosome biogenesis as a promising cancer therapeutic strategy.

show abstract

Section: Ca 2+ Signalingmentioning

confidence: 99%

Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Although chemotherapy is an effective method to treat cancer, the resistance of tumor cells to chemotherapeutic drugs often leads to treatment failure [15,16]. Therefore, understanding the resistance mechanism of Ptx in ovarian cancer may contribute to seeking anti-Ptx resistance targets, thereby improving the clinical efficacy of Ptx.…”

Section: Discussionmentioning

confidence: 99%

CircSETDB1 contributes to paclitaxel resistance of ovarian cancer cells by sponging miR-508-3p and regulating ABCC1 expression

Huang

Chen

et al. 2022

Anti-Cancer Drugs

View full text Add to dashboard Cite

Ovarian cancer is a gynecological tumor with a poor prognosis. The chemotherapy failure and recurrence induced by paclitaxel (Ptx) resistance are the main reason for the failure of ovarian cancer treatment. In this study, we aimed to explore the role of circular RNA (circRNA) in the regulation of Ptx resistance in ovarian cancer. Quantitative reverse transcription PCR was performed to detect the expression of circRNA SET domain bifurcated histone lysine methyltransferase 1 (circSETDB1), microRNA (miR)-508-3p and ATP-binding cassette subfamily C member 1 (ABCC1) mRNA. The effects of circSETDB1 on Ptx resistance were explored by cell counting kit-8, 5-ethynyl-2′-deoxyuridine, and flow cytometry experiments in vitro. The protein level was assessed by western blot. Dual-luciferase reporter and RNA pull-down assays were carried out to confirm the interactions among circSETDB1, miR-508-3p, and ABCC1. Xenograft tumor experiment was performed to investigate the effect of circSETDB1 on Ptx resistance in vivo. CircSETDB1 was highly expressed in Ptx-resistant ovarian cancer. CircSETDB1 knockdown inhibited cell proliferation viability, half maximal inhibitory concentration value of Ptx, cell cycle progression, and induced cell apoptosis in Ptx-resistant ovarian cancer cells. miR-508-3p was a target of circSETDB1, and inhibition of miR-508-3p overturned the effects of circSETDB1 knockdown on the Ptx resistance of ovarian cancer cells. miR-508-5p could bind to ABCC1. Overexpression of ABCC1 reversed the effects of circSETDB1 knockdown on the Ptx resistance of ovarian cancer cells. CircSETDB1 knockdown also enhanced Ptx sensitivity in vivo. In conclusion, circSETDB1 regulated Ptx resistance of ovarian cancer by targeting miR-508-3p/ABCC1 axis.

show abstract

“…Our Table 4 provides a range of examples of compounds/drugs that have been found to exert an impact on the functional outcome in vitro or in vivo in diverse blood cancer types. Some of these compounds are in clinical use for other applications or undergo pre-clinical/clinical testing in solid tumors ( 394 , 395 ). If their targets are found to be pathogenic in blood cancer, these drugs could be rapidly transitioned to hematologic applications.…”

Section: Discussionmentioning

confidence: 99%

Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential

Immanuel

Li²,

Green³

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

Intracellular calcium signaling regulates diverse physiological and pathological processes. In solid tumors, changes to calcium channels and effectors via mutations or changes in expression affect all cancer hallmarks. Such changes often disrupt transport of calcium ions (Ca2+) in the endoplasmic reticulum (ER) or mitochondria, impacting apoptosis. Evidence rapidly accumulates that this is similar in blood cancer. Principles of intracellular Ca2+ signaling are outlined in the introduction. We describe different Ca2+-toolkit components and summarize the unique relationship between extracellular Ca2+ in the endosteal niche and hematopoietic stem cells. The foundational data on Ca2+ homeostasis in red blood cells is discussed, with the demonstration of changes in red blood cell disorders. This leads to the role of Ca2+ in neoplastic erythropoiesis. Then we expand onto the neoplastic impact of deregulated plasma membrane Ca2+ channels, ER Ca2+ channels, Ca2+ pumps and exchangers, as well as Ca2+ sensor and effector proteins across all types of hematologic neoplasms. This includes an overview of genetic variants in the Ca2+-toolkit encoding genes in lymphoid and myeloid cancers as recorded in publically available cancer databases. The data we compiled demonstrate that multiple Ca2+ homeostatic mechanisms and Ca2+ responsive pathways are altered in hematologic cancers. Some of these alterations may have genetic basis but this requires further investigation. Most changes in the Ca2+-toolkit do not appear to define/associate with specific disease entities but may influence disease grade, prognosis, treatment response, and certain complications. Further elucidation of the underlying mechanisms may lead to novel treatments, with the aim to tailor drugs to different patterns of deregulation. To our knowledge this is the first review of its type in the published literature. We hope that the evidence we compiled increases awareness of the calcium signaling deregulation in hematologic neoplasms and triggers more clinical studies to help advance this field.

show abstract

Targeting Ca2+ signaling: A new arsenal against cancer

Cited by 17 publications

References 116 publications

Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer

Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer

CircSETDB1 contributes to paclitaxel resistance of ovarian cancer cells by sponging miR-508-3p and regulating ABCC1 expression

Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential

Contact Info

Product

Resources

About