Targeting the tumor stroma for cancer therapy

Xu, Maosen; Zhang, Tao; Xia, Rong; Wei, Yuquan; Wei, Xiawei

doi:10.1186/s12943-022-01670-1

Cited by 107 publications

(87 citation statements)

References 514 publications

(540 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therapeutic approaches to CAFs and MSCs are expertly reviewed elsewhere [ 25 , 26 , 46 , 352 , 506 , 507 , 508 ]. A significant body of literature discusses the potential of targeting cancer stroma, and specifically CAFs.…”

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

“…Chemotherapy, biotherapy, or radiation therapy can, in some cases, reverse the protumorigenic effects of CAFs [ 25 , 26 , 46 , 352 , 506 , 507 , 508 ]. Disruption of growth factor signaling was an approach taken in one study, where antisense oligonucleotides targeting HGF, which was secreted by CAFs, inhibited VEGF production and CAF-induced increase in clonogenic potential in co-cultured tumor cells [ 453 ].…”

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

“…Inhibiting desmoplasia with chemokine inhibitors may have more pronounced effects in tumors that are more desmoplastic, such as ER + breast tumors [ 590 ]. Clinical trials targeting CAFs, MSCs, and pericytes have had modest successes in prolonging survival, but due to CAF heterogeneity and concerns of opposing effects on cancer progression, global approaches must be abandoned for more specific targeted approaches that perhaps address cancer cell and CAF survival mechanisms in concert [ 508 ]. A systematic review and meta-analysis of twenty clinical studies and six randomized controlled trials of anti-VEGF/VEGFR therapy revealed a treatment advantage of combined therapy with nab-paclitaxel, with the only marginal improvement of objective response rates and progression-free survival, but not overall survival [ 592 ].…”

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

See 2 more Smart Citations

Fibroblasts as Turned Agents in Cancer Progression

Wieder

2023

Cancers

View full text Add to dashboard Cite

Differentiated epithelial cells reside in the homeostatic microenvironment of the native organ stroma. The stroma supports their normal function, their G0 differentiated state, and their expansion/contraction through the various stages of the life cycle and physiologic functions of the host. When malignant transformation begins, the microenvironment tries to suppress and eliminate the transformed cells, while cancer cells, in turn, try to resist these suppressive efforts. The tumor microenvironment encompasses a large variety of cell types recruited by the tumor to perform different functions, among which fibroblasts are the most abundant. The dynamics of the mutual relationship change as the sides undertake an epic battle for control of the other. In the process, the cancer “wounds” the microenvironment through a variety of mechanisms and attracts distant mesenchymal stem cells to change their function from one attempting to suppress the cancer, to one that supports its growth, survival, and metastasis. Analogous reciprocal interactions occur as well between disseminated cancer cells and the metastatic microenvironment, where the microenvironment attempts to eliminate cancer cells or suppress their proliferation. However, the altered microenvironmental cells acquire novel characteristics that support malignant progression. Investigations have attempted to use these traits as targets of novel therapeutic approaches.

show abstract

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

Section: Cancer Stroma As a Therapeutic Targetmentioning

confidence: 99%

See 1 more Smart Citation

Fibroblasts as Turned Agents in Cancer Progression

Wieder

2023

Cancers

View full text Add to dashboard Cite

show abstract

“…It attenuates the efficacy of immunotherapy by depleting specific T cell populations and attenuating the sensitization of T cells [ 21 ]. Fortunately, the tumor microenvironment is dynamic [ 22 ]. The dynamic regulation and interactions of various immune cells therein can also significantly influence the malignant properties of tumor cells.…”

Section: Immunoregulation and Tumor Microenvironmentmentioning

confidence: 99%

The Role of Cytoskeleton Protein 4.1 in Immunotherapy

Yuan

Chen

et al. 2023

IJMS

View full text Add to dashboard Cite

Cytoskeleton protein 4.1 is an essential class of skeletal membrane protein, initially found in red blood cells, and can be classified into four types: 4.1R (red blood cell type), 4.1N (neuronal type), 4.1G (general type), and 4.1B (brain type). As research progressed, it was discovered that cytoskeleton protein 4.1 plays a vital role in cancer as a tumor suppressor. Many studies have also demonstrated that cytoskeleton protein 4.1 acts as a diagnostic and prognostic biomarker for tumors. Moreover, with the rise of immunotherapy, the tumor microenvironment as a treatment target in cancer has attracted great interest. Increasing evidence has shown the immunoregulatory potential of cytoskeleton protein 4.1 in the tumor microenvironment and treatment. In this review, we discuss the role of cytoskeleton protein 4.1 within the tumor microenvironment in immunoregulation and cancer development, with the intention of providing a new approach and new ideas for future cancer diagnosis and treatment.

show abstract

“…Cancer is also known as the wound that never heals ( 77 ). It has been proved that MSCs can be recruited to the tumor sites and transform into tumor-associated MSCs (TAMSCs) or differentiate into CAFs to affect the progression of the cancer ( 78 , 79 ).…”

Section: The Microenvironment Of Colorectal Cscsmentioning

confidence: 99%

Ecological niches for colorectal cancer stem cell survival and thrival

Che

2023

Front. Oncol.

View full text Add to dashboard Cite

To date, colorectal cancer is still ranking top three cancer types severely threatening lives. According to cancer stem cell hypothesis, malignant colorectal lumps are cultivated by a set of abnormal epithelial cells with stem cell-like characteristics. These vicious stem cells are derived from intestinal epithelial stem cells or transformed by terminally differentiated epithelial cells when they accumulate an array of transforming genomic alterations. Colorectal cancer stem cells, whatever cell-of-origin, give rise to all morphologically and functionally heterogenous tumor daughter cells, conferring them with overwhelming resilience to intrinsic and extrinsic stresses. On the other hand, colorectal cancer stem cells and their daughter cells continuously participate in constructing ecological niches for their survival and thrival by communicating with adjacent stromal cells and circulating immune guardians. In this review, we first provide an overview of the normal cell-of-origin populations contributing to colorectal cancer stem cell reservoirs and the niche architecture which cancer stem cells depend on at early stage. Then we survey recent advances on how these aberrant niches are fostered by cancer stem cells and their neighbors. We also discuss recent research on how niche microenvironment affects colorectal cancer stem cell behaviors such as plasticity, metabolism, escape of immune surveillance as well as resistance to clinical therapies, therefore endowing them with competitive advantages compared to their normal partners. In the end, we explore therapeutic strategies available to target malignant stem cells.

show abstract

Targeting the tumor stroma for cancer therapy

Cited by 107 publications

References 514 publications

Fibroblasts as Turned Agents in Cancer Progression

Fibroblasts as Turned Agents in Cancer Progression

The Role of Cytoskeleton Protein 4.1 in Immunotherapy

Ecological niches for colorectal cancer stem cell survival and thrival

Contact Info

Product

Resources

About