Chemotherapy-induced metastasis: molecular mechanisms and clinical therapies

Su, J.; Li, Shaozhi; Zhou, Xiaofeng; Zhang, Zhijing; Ye, Yu; Liu, S.; Qi, Qi

doi:10.1038/s41401-023-01093-8

Cited by 16 publications

(10 citation statements)

References 162 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They postulated, just as we do here, that cell physical phenotyping is a complementary prognostic tool that could guide treatment strategies and therapeutic interventions. Already, the mechanisms of chemotherapy-induced metastasis so far uncovered and new therapeutic strategies suggest the importance of biophysical aspects [ 21 , 22 , 23 , 24 , 25 ]. More concretely, multidrug chemotherapy regimens may have to include drugs that tune cell biophysical properties in antimetastatic ways.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, following our work, several research groups reported that certain chemotherapeutics elicit a de novo prometastatic tumor microenvironment in both preclinical studies and in some patient subpopulations [ 14 , 15 , 16 , 17 , 18 , 19 ]. Expectedly, the very notion of chemotherapy-induced metastasis was initially disconcerting since chemotherapy is one of the main pillars of cancer treatment, but the aforementioned overwhelming evidence as well as newer clinical case reports [ 20 ] have not only led to a concerted search for the causal mechanisms but also to new therapeutic strategies aimed at mitigating chemotherapy-induced metastasis [ 21 , 22 , 23 , 24 , 25 ]. Some of the mechanisms of chemotherapy-induced metastasis reported include increase in extravasation and intravasation [ 15 ], increase in intravasation sites called tumor microenvironments of metastasis (TMEM) [ 16 ], increased migration and release of circulating tumor cells into the blood stream of cancer patients following chemotherapy [ 17 ], increased infiltration of immune cells such as neutrophils [ 18 ] and release of prometastatic proteins through extra-cellular vesicles [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Microfluidic Microcirculation Mimetic for Exploring Biophysical Mechanisms of Chemotherapy-Induced Metastasis

Abraham,

Virdi,

Herrero

et al. 2023

Micromachines

View full text Add to dashboard Cite

There is rapidly emerging evidence from pre-clinical studies, patient samples and patient subpopulations that certain chemotherapeutics inadvertently produce prometastatic effects. Prior to this, we showed that doxorubicin and daunorubicin stiffen cells before causing cell death, predisposing the cells to clogging and extravasation, the latter being a step in metastasis. Here, we investigate which other anti-cancer drugs might have similar prometastatic effects by altering the biophysical properties of cells. We treated myelogenous (K562) leukemic cancer cells with the drugs nocodazole and hydroxyurea and then measured their mechanical properties using a microfluidic microcirculation mimetic (MMM) device, which mimics aspects of blood circulation and enables the measurement of cell mechanical properties via transit times through the device. We also quantified the morphological properties of cells to explore biophysical mechanisms underlying the MMM results. Results from MMM measurements show that nocodazole- and hydroxyurea-treated K562 cells exhibit significantly altered transit times. Nocodazole caused a significant (p < 0.01) increase in transit times, implying a stiffening of cells. This work shows the feasibility of using an MMM to explore possible biophysical mechanisms that might contribute to chemotherapy-induced metastasis. Our work also suggests cell mechanics as a therapeutic target for much needed antimetastatic strategies in general.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Microfluidic Microcirculation Mimetic for Exploring Biophysical Mechanisms of Chemotherapy-Induced Metastasis

Abraham,

Virdi,

Herrero

et al. 2023

Micromachines

View full text Add to dashboard Cite

show abstract

“…Systemic chemotherapy, the first line of treatment for metastatic cancer, fails to target metastatic cancer cells; has other serious side effects such as off-target accumulation, toxicity, and rapid renal and hepatic clearance; and has the potential to induce metastasis. 2,3 It has been reported that over 90% of failures in chemotherapy occur during the invasion and metastasis of cancers. 4 Recently, advanced treatment options such as immunotherapy, epigenome-modifying agents, and combination therapy have reduced toxicity in metastatic cancer patients but have limited efficacy in inhibiting tumor metastasis.…”

Section: Introductionmentioning

confidence: 99%

Hydrogels as local depots for on-demand therapeutic delivery: potential therapeutic approaches for tumor metastasis

Andrgie,

Tsai

2024

Mater. Adv.

View full text Add to dashboard Cite

show abstract

“…As the mechanism of treatment-induced metastasis is beyond the scope of this perspective, we will not discuss it in depth. Several recent reviews have discussed in detail the current clinical observations, potential molecular mechanisms, and prevention strategies for treatment-induced metastasis ( Karagiannis et al, 2019 ; Shaked, 2019 ; Su et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Improving the predictive accuracy of efficacy evaluation using tumor orthotopic transplant and resection model

Li,

Luo,

Qian

2024

Front. Pharmacol.

View full text Add to dashboard Cite

Preclinical efficacy evaluation and tumor drug sensitivity analysis are two main applications of efficacy evaluation. Preclinical efficacy evaluation is to predict whether candidate drugs or therapies may improve patient outcomes in clinical trials. Tumor drug sensitivity analysis is an approach for the personalized evaluation and optimization of approved anti-cancer drugs and treatment regimens. Overall survival (OS) is the gold standard to evaluate the outcome of drugs or therapies in both clinical trials and clinical treatment. Many efficacy evaluation models, such as cell model, tumor cell-line transplant model, patient-derived tumor xenograft model, tumor organoid model, have been developed to assess the inhibitory effect of tested drugs or therapies on tumor growth. In fact, many treatments may also lead to malignant progression of tumors, such as chemotherapy, which can lead to metastasis. Therefore, tumor growth inhibition does not necessarily predict OS benefit. Whether it can prevent or inhibit tumor recurrence and metastasis is the key to whether drugs and therapies can improve patient outcomes. In this perspective, we summarize the current understanding of the pathological progression of tumor recurrence and metastasis, point out the shortcomings of existing tumor transplant models for simulating the clinical scenario of malignant progression of tumors, and propose five improved indicators for comprehensive efficacy evaluation to predict OS benefit using tumor orthotopic transplant and resection model. Improvement in the accuracy of efficacy evaluation will accelerate the development process of anti-cancer drugs or therapies, optimize treatment regimens to improve OS benefit, and reduce drug development and cancer treatment costs.

show abstract

Chemotherapy-induced metastasis: molecular mechanisms and clinical therapies

Cited by 16 publications

References 162 publications

Microfluidic Microcirculation Mimetic for Exploring Biophysical Mechanisms of Chemotherapy-Induced Metastasis

Microfluidic Microcirculation Mimetic for Exploring Biophysical Mechanisms of Chemotherapy-Induced Metastasis

Hydrogels as local depots for on-demand therapeutic delivery: potential therapeutic approaches for tumor metastasis

Improving the predictive accuracy of efficacy evaluation using tumor orthotopic transplant and resection model

Contact Info

Product

Resources

About