Emerging Role of Autophagy in Governing Cellular Dormancy, Metabolic Functions, and Therapeutic Responses of Cancer Stem Cells DOI Creative Commons
Meenakshi Tiwari,

Pransu Srivastava,

Sabiya Abbas

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(5), P. 447 - 447

Published: March 4, 2024

Tumors are composed of heterogeneous populations dysregulated cells that grow in specialized niches support their growth and maintain properties. Tumor heterogeneity metastasis among the major hindrances exist while treating cancer patients, leading to poor clinical outcomes. Although factors determine tumor complexity remain largely unknown, several genotypic phenotypic changes, including DNA mutations metabolic reprograming provide with a survival advantage over host resistance therapeutics. Furthermore, presence specific population within mass, commonly known as stem (CSCs), is thought initiate formation, maintenance, resistance, recurrence. Therefore, these CSCs have been investigated detail recently potential targets treat prevent Understanding molecular mechanisms involved CSC proliferation, self-renewal, dormancy may important clues for developing effective therapeutic strategies. Autophagy, catabolic process, has long recognized regulate various physiological pathological processes. In addition regulating cells, recent studies identified critical role autophagy functions. Autophagy activated under adverse conditions promotes cellular survival, even cell death. Thus, it intriguing address whether or inhibits functions modulation can be used functions, either alone combination. This review describes roles regulation proliferation quiescence CSCs, its during stress. The further highlights autophagy-associated pathways could CSCs. Overall, present will help rationalize translational approaches involve autophagy-mediated controlling progression, metastasis,

Language: Английский

Targeting autophagy and lipid metabolism in cancer stem cells DOI

Bandana Chakravarti,

Jawed A. Siddiqui, Rohit A. Sinha

et al.

Biochemical Pharmacology, Journal Year: 2023, Volume and Issue: 212, P. 115550 - 115550

Published: April 13, 2023

Language: Английский

Citations

17
Intricate relationship between cancer stemness, metastasis, and drug resistance DOI Creative Commons
Tikam Chand Dakal, Ravi Bhushan, Caiming Xu

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(10)

Published: Sept. 21, 2024

Cancer stem cells (CSCs) are widely acknowledged as the drivers of tumor initiation, epithelial-mesenchymal transition (EMT) progression, and metastasis. Originating from both hematologic solid malignancies, CSCs exhibit quiescence, pluripotency, self-renewal akin to normal cells, thus orchestrating heterogeneity growth. Through a dynamic interplay with microenvironment (TME) intricate signaling cascades, undergo transitions differentiated cancer culminating in therapy resistance disease recurrence. This review undertakes an in-depth analysis multifaceted mechanisms underlying stemness CSC-mediated therapy. Intrinsic factors encompassing TME, hypoxic conditions, oxidative stress, alongside extrinsic processes such drug efflux mechanisms, collectively contribute therapeutic resistance. An exploration into key pathways, including JAK/STAT, WNT, NOTCH, HEDGEHOG, sheds light on their pivotal roles sustaining phenotypes. Insights gleaned preclinical clinical studies hold promise refining discovery efforts optimizing interventions, especially chimeric antigen receptor (CAR)-T cell therapy, cytokine-induced killer (CIK) natural (NK) cell-mediated CSC-targeting others. Ultimately use sorting single sequencing approaches for elucidating fundamental characteristics inherent will enhance our comprehension CSC intratumor heterogeneity, which ultimately would inform about tailored personalized interventions.

Language: Английский

Citations

8
Exosome crosstalk between cancer stem cells and tumor microenvironment: cancer progression and therapeutic strategies DOI Creative Commons
Qi Li, Guangpeng He, Yifan Yu

et al.

Stem Cell Research & Therapy, Journal Year: 2024, Volume and Issue: 15(1)

Published: Nov. 22, 2024

Abstract Cancer stem cells (CSCs) represent a small yet pivotal subset of tumor endowed with self-renewal capabilities. These are intricately linked to progression and central drug resistance, metastasis, recurrence. The microenvironment (TME) encompasses the cancer their surrounding milieu, including immune inflammatory cells, cancer-associated fibroblasts, adjacent stromal tissues, vasculature, variety cytokines chemokines. Within TME, such as endothelial adipocytes, fibroblasts release growth factors, cytokines, chemokines, exosomes, which can either sustain or disrupt CSCs, thereby influencing progression. Conversely, CSCs also secrete affecting various components TME. Exosomes, extracellular vesicles (EVs), carry complex cargo nucleic acids, proteins, lipids, playing crucial role in communication between This review primarily focuses on impact exosomes secreted by (CSC-exo) progression, roles maintaining stemness, promoting angiogenesis, facilitating inducing suppression, contributing resistance. Additionally, we discuss how different within TME affect CSCs. Finally, explore potential utilizing mitigate detrimental effects target eliminate them. A thorough understanding exosome-mediated crosstalk could provide valuable insights for developing targeted therapies against

Language: Английский

Citations

8
CSNK2A1 confers gemcitabine resistance to pancreatic ductal adenocarcinoma via inducing autophagy DOI Creative Commons
Zhide Liu,

Yin-Hao Shi,

Qiong‐Cong Xu

et al.

Cancer Letters, Journal Year: 2024, Volume and Issue: 585, P. 216640 - 216640

Published: Jan. 28, 2024

Gemcitabine, a pivotal chemotherapeutic agent for pancreatic ductal adenocarcinoma (PDAC), frequently encounters drug resistance, posing significant clinical challenge with implications PDAC patient prognosis. In this study, employing an integrated approach involving bioinformatic analyses from multiple databases, we unveil CSNK2A1 as key regulatory factor. The patient-derived xenograft (PDX) model further substantiates the critical role of in gemcitabine resistance within context PDAC. Additionally, targeted silencing expression significantly enhances sensitivity cells to treatment. Mechanistically, CSNK2A1's transcriptional regulation is mediated by H3K27 acetylation Moreover, identify activator autophagy, and enhanced autophagy drives resistance. Silmitasertib, established inhibitor, can effectively inhibit autophagy. Notably, combinatorial treatment Silmitasertib demonstrates remarkable efficacy treating summary, our study reveals potent predictive factor inhibition represents promising therapeutic strategy restore PDAC, offering hope improved outcomes.

Language: Английский

Citations

6
Emerging Role of Autophagy in Governing Cellular Dormancy, Metabolic Functions, and Therapeutic Responses of Cancer Stem Cells DOI Creative Commons
Meenakshi Tiwari,

Pransu Srivastava,

Sabiya Abbas

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(5), P. 447 - 447

Published: March 4, 2024

Tumors are composed of heterogeneous populations dysregulated cells that grow in specialized niches support their growth and maintain properties. Tumor heterogeneity metastasis among the major hindrances exist while treating cancer patients, leading to poor clinical outcomes. Although factors determine tumor complexity remain largely unknown, several genotypic phenotypic changes, including DNA mutations metabolic reprograming provide with a survival advantage over host resistance therapeutics. Furthermore, presence specific population within mass, commonly known as stem (CSCs), is thought initiate formation, maintenance, resistance, recurrence. Therefore, these CSCs have been investigated detail recently potential targets treat prevent Understanding molecular mechanisms involved CSC proliferation, self-renewal, dormancy may important clues for developing effective therapeutic strategies. Autophagy, catabolic process, has long recognized regulate various physiological pathological processes. In addition regulating cells, recent studies identified critical role autophagy functions. Autophagy activated under adverse conditions promotes cellular survival, even cell death. Thus, it intriguing address whether or inhibits functions modulation can be used functions, either alone combination. This review describes roles regulation proliferation quiescence CSCs, its during stress. The further highlights autophagy-associated pathways could CSCs. Overall, present will help rationalize translational approaches involve autophagy-mediated controlling progression, metastasis,

Language: Английский

Citations

6