S100A8 promotes chemoresistance via augmenting autophagy in B‑cell lymphoma cells

Zhang, Li; Zhou, Shunhua; Zhou, Tiejun; Yuan, Kaifeng; Li, Xiaoming; Tang, Junling

doi:10.3892/or.2020.7841

Cited by 8 publications

(3 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The levels of S100A8/A9 in saliva can help differentiate the subgroups of Sjögren’s syndrome with lymphoma risk ( 44 ). A recent report found that S100A8 could promote chemoresistance to adriamycin and vincristine by enhancing autophagy in B-cell lymphoma cells ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

iTRAQ-Based Proteomic Analysis Reveals Potential Serum Biomarkers for Pediatric Non-Hodgkin’s Lymphoma

Yang

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

Non-Hodgkin’s lymphoma (NHL) is the third most common malignant tumor among children. However, at initial NHL diagnosis, most cases are at an advanced stage because of nonspecific clinical manifestations and currently limited diagnostic methods. This study aimed to screen and verify potential serum biomarkers of pediatric NHL using isobaric tags for relative and absolute quantification (iTRAQ)-based proteomic analysis. Serum protein expression profiles from children with B-NHL (n=20) and T-NHL (n=20) and healthy controls (n=20) were detected by utilizing iTRAQ in combination with two-dimensional liquid chromatography-tandem mass spectrometry (2D LC–MS/MS) and analyzed by applying Ingenuity Pathway Analysis (IPA). The candidate biomarkers S100A8 and LRG1 were further validated by using enzyme-linked immunosorbent assays (ELISAs). Receiver operating characteristic (ROC) analysis based on ELISA data was used to evaluate diagnostic efficacy. In total, 534 proteins were identified twice using iTRAQ combined with 2D LC–MS/MS. Further analysis identified 79 and 73 differentially expressed proteins in B-NHL and T-NHL serum, respectively, compared with control serum according to our defined criteria; 34 proteins were overexpressed and 45 proteins underexpressed in B-NHL, whereas 45 proteins were overexpressed and 28 proteins underexpressed in T-NHL (p < 0.05). IPA demonstrated a variety of signaling pathways, including acute phase response signaling and liver X receptor/retinoid X receptor (LXR/RXR) activation, to be strongly associated with pediatric NHL. S100A8 and LRG1 were elevated in NHL patients compared to normal controls according to ELISA (p < 0.05), which was consistent with iTRAQ results. The areas under the ROC curves of S100A8, LRG1, and the combination of S100A8 and LRG1 were 0.873, 0.898 and 0.970, respectively. Our findings indicate that analysis of the serum proteome using iTRAQ combined with 2D LC–MS/MS is a feasible approach for biomarker discovery. Serum S100A8 and LRG1 are promising candidate biomarkers for pediatric NHL, and these differential proteins illustrate a novel pathogenesis and may be clinically helpful for NHL diagnosis in the future.

show abstract

Section: Discussionmentioning

confidence: 99%

iTRAQ-Based Proteomic Analysis Reveals Potential Serum Biomarkers for Pediatric Non-Hodgkin’s Lymphoma

Yang

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…S100- A8 and A9 are expressed constitutively in the cytoplasm of myeloid cells, including myeloid precursors, but are absent from lymphocytes ( 301 ). Increased activity of multiple S100 family members is associated with increased drug resistance in hematologic malignancies including AML, CML, ALL, and B-cell lymphomas ( 302 , 303 ). For example, S100-A8/A9 contribute to gilteritinib resistance in FLT3- internal tandem duplications- (FLT3-ITD)-positive AML primary cells and cell lines ( 304 ).…”

Section: Calcium Signaling Deregulation In Blood Cancermentioning

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

“…They reported that S100A8 increased drug resistance through the stimulation of BECN1-PI3KC3 and BECN1-BCL-2 complex formation, prompting early mitophagic signaling. In addition, S100A8 enhanced BNIP3 expression, boosting mitophagic signaling activation [ 223 ]. BNIP3 is a 19 kDa BH3-only protein located at the mitochondria-ER interface; specifically, it is anchored to the OMM through the C-terminal domain, while its N-terminal domain points to the cytoplasm.…”

Section: Role Of Proteins That Regulate Mitochondrial Ca 2+ Homeostasis In Cancer Chemoresistance and Death Resistancementioning

confidence: 99%

Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance

Genovese

Carinci

Modesti

et al. 2021

IJMS

View full text Add to dashboard Cite

Mitochondria are key regulators of cell survival and are involved in a plethora of mechanisms, such as metabolism, Ca2+ signaling, reactive oxygen species (ROS) production, mitophagy and mitochondrial transfer, fusion, and fission (known as mitochondrial dynamics). The tuning of these processes in pathophysiological conditions is fundamental to the balance between cell death and survival. Indeed, ROS overproduction and mitochondrial Ca2+ overload are linked to the induction of apoptosis, while the impairment of mitochondrial dynamics and metabolism can have a double-faceted role in the decision between cell survival and death. Tumorigenesis involves an intricate series of cellular impairments not yet completely clarified, and a further level of complexity is added by the onset of apoptosis resistance mechanisms in cancer cells. In the majority of cases, cancer relapse or lack of responsiveness is related to the emergence of chemoresistance, which may be due to the cooperation of several cellular protection mechanisms, often mitochondria-related. With this review, we aim to critically report the current evidence on the relationship between mitochondria and cancer chemoresistance with a particular focus on the involvement of mitochondrial dynamics, mitochondrial Ca2+ signaling, oxidative stress, and metabolism to possibly identify new approaches or targets for overcoming cancer resistance.

show abstract

S100A8 promotes chemoresistance via augmenting autophagy in B‑cell lymphoma cells

Cited by 8 publications

References 48 publications

iTRAQ-Based Proteomic Analysis Reveals Potential Serum Biomarkers for Pediatric Non-Hodgkin’s Lymphoma

iTRAQ-Based Proteomic Analysis Reveals Potential Serum Biomarkers for Pediatric Non-Hodgkin’s Lymphoma

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

Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance

Contact Info

Product

Resources

About