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Editorial
. 2022 Aug 26:13:46-48.
doi: 10.18632/genesandcancer.222. eCollection 2022.

Splice modulating oligomers as cancer therapeutics

KuanHui E Chen, Ameae M Walker
Editorial

Splice modulating oligomers as cancer therapeutics

KuanHui E Chen et al. Genes Cancer. .
No abstract available

Keywords: T regulatory cells; dominant negatives; prolactin receptors; receptor isoforms; tumor microenvironment.

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Conflict of interest statement

CONFLICTS OF INTEREST The University of California, Riverside holds the patent for this approach and KEC and AMW are inventors.

Figures

Figure 1
Figure 1. Tumor-T regulatory cell interactions.
Syngeneic, triple negative mouse breast tumors attract T regulatory cells (Treg) out of the circulation (A) into the complex microenvironment of the tumor (B). All cell types in the tumor can express PRLR (shown in red), but some only when/if activated. The cells constituting the tumor parenchyma overexpress the long form of the PRLR (LF PRLR, shown in red with a longer intracellular portion) which promotes proliferation and survival. These parenchymal cells (and possibly other cells) produce CCL17, which attracts the Tregs from the circulation. Tregs suppress the function of anti-tumor effector cells (CD8+, CD4+, NK) and promote expression of mesenchymal genes in the parenchymal cells, thereby facilitating metastatic spread. Knockdown of the LF PRLR has differentiation and apoptotic promoting effects on the tumor parenchyma, amplified through the relative increase in the short forms of the PRLR, and reduces recruitment of Tregs, allowing activation of effector cells [10, 11]. Each dot in panel A represents an individual animal; ****p = 5.8 × 10−8; the green arrow represents the reciprocal influences between tumor cells and Tregs.
See this image and copyright information in PMC

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