Page 194 - EJMO-9-1

Eurasian Journal of Medicine and
Oncology
Research on hypoxia and ECM in cancer

the direct role of HIF-1α expression in lung cancer cells for assessing cancer invasiveness and guiding treatment
in inhibiting TGF-β-induced EMT. The low survival strategies. McKenzie et al. found that the ECM
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rate of lung cancer is due to late diagnosis and tumor tumor suppressor maspin is overexpressed under hypoxia
heterogeneity, which reduces treatment efficacy. Sarma in prostate cancer cells, enhancing hypoxia-induced
et al. suggested that personalized adjuvant therapy apoptosis without significantly affecting cell migration.
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combined with targeted nanocarrier drug delivery systems This effect leads to the inhibition of tumor growth and
can improve therapeutic outcomes. Functionalized angiogenesis, potentially by targeting Akt and focal
nanocarriers enhance cellular uptake, immune evasion, adhesion kinase. Rahbari et al. discovered that anti-
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and penetration into TME, modulating ECM, CAF, and vascular endothelial growth factor (VEGF) therapy in
TAM receptors to bypass the TME and achieve precise metastatic colorectal cancer induces ECM remodeling,
targeting, potentially improving treatment efficacy for altering the physical properties of liver metastases. The
non-small-cell lung cancer (NSCLC). 99 treatment resulted in increased hyaluronic acid (HA)
and sulfated glycosaminoglycans within the tumor, with
4.4. GBM
minimal changes in collagen deposition. The increase in
Hypoxia promotes the development of GBM by regulating HA correlated with increased tumor stiffness, potentially
hypoxia-responsive gene networks (HRGs). Mao et al. driven by tumor hypoxia. Enzymatic removal of HA
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identified CEBPD as a key transcription factor through improved blood flow perfusion post-treatment and, when
proteomics and transcription factor analyses. CEBPD combined with anti-VEGF therapy and chemotherapy,
was found to regulate most HRGs and hypoxia-regulated extended survival. 105
proteins, with its high expression under hypoxic conditions
closely linked to GBM invasiveness and poor prognosis. 5. Conclusion
CEBPD advances tumor progression by activating FN1 and Our research offers a comprehensive visualization of the
the EGFR/PI3K pathway, highlighting CEBPD as a central relevant literature on hypoxia and ECM. The USA holds
regulatory factor within the GBM hypoxia gene network a dominant position in research depth and international
that mediates EGFR phosphorylation through ECM to collaboration, despite China leading in the sheer volume of
activate the EGFR/PI3K pathway. Miroshnikova et al. publications. Institutions, such as Johns Hopkins University
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indicate that IDH1 mutations reduce glioma invasiveness and Harvard University, which have the highest citation
by suppressing HIF1α-dependent TNC expression, frequencies, exert significant influence in this domain. This
which, in turn, decreases ECM stiffness. Recurrent IDH1- field is currently experiencing rapid growth, with recent
mutant gliomas exhibit higher ECM stiffness, partly due research focusing heavily on CAFs. Research on hypoxia
to weakened miR-203 inhibition of HIF1α and TNC. and ECM in cancer is mainly focusing on pancreatic
Increased ECM stiffness promotes GBM invasiveness and cancer, lung cancer, GBM multiforme, and breast cancer.
contributes to tumor recurrence. 101
Moreover, clinical therapy resistance for TNBC, closely
4.5. Other cancers associated with the ECM, is expected to be a key focal
point in the future. This work highlights the cutting-
Tse et al. discovered that the HBV protein HBx promotes edge dynamics and future trajectories in cancer research,
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the expression of the LOX gene family in hepatocellular providing researchers with an intuitive understanding
carcinoma (HCC) by stabilizing the transcription factor of current progress, potential collaborations, and
HIF-1α. The LOX family proteins enhance collagen opportunities for further academic exchange.
crosslinking, thereby driving cancer progression and
metastasis. Knockdown of HBx reduces collagen This study visualized the relationship between hypoxia
crosslinking and cancer cell invasion, inhibiting HCC and ECM in cancer, using bibliometrics to understand
growth and metastasis. This suggests that HBx promotes research trends and hotspots. However, this study has
HCC metastasis through the HIF-1α/LOX pathway by limitations. For instance, due to the current limitations
remodeling the ECM. Penet et al. compared the of scientific measurement software, it is a challenge to
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ECM of orthotopic and subcutaneous prostate tumors, analyze data from multiple databases simultaneously.
finding a significant increase in CAFs and collagen type I Therefore, this study solely relied on the WOSCC
(Col1) fibers in orthotopic tumors. The accumulation of database. In addition, this study only included articles and
alb-GdDTPA in orthotopic tumors was also significantly reviews, excluding abstracts, conference papers, or books.
higher than that in subcutaneous tumors, indicating the Hence, future research can be conducted using more
critical role of CAFs in prostate cancer metastasis. They comprehensive databases for a more comprehensive and
suggest that ECM characterization could be valuable accurate analysis.

Volume 9 Issue 1 (2025) 186 doi: 10.36922/ejmo.7116