The male gonads are the testes, which are housed in the scrotum. The testes produce sperm (male gametes) and testosterone (the main male hormone). Following production in the testes, sperm move through the epididymis and into the vas deferens, both tubules that contain sperm until ejaculation. Lastly, the prostate is a male reproductive gland that produces the fluid that makes up semen.

The female reproductive system is composed of the ovaries, fallopian tubes, uterus, and vagina. Eggs (female gametes) mature in the ovaries, where estrogen (the main female hormone) is also produced. Once per month, an egg is released into the fallopian tubes, where it travels into the uterus. If fertilized, a fetus develops. Once fully developed, the fetus exits the uterus via the vaginal canal.

Recent Research Using Lifeline® Prostate Epithelial Cells and Uterine Smooth Muscle Cells

Efforts to develop diagnostic screening methods for cancer have increased in recent years. The ability to detect cancer biomarkers through a simple blood or urine test has great promise, but identifying reliable biomarkers has proven challenging. To date, prostate-specific antigen (PSA) has served as a biomarker for prostate cancer, but has not proven consistently accurate. Therefore, Narain et al. set out to address the need for additional biomarkers using systems biology analysis of the secretome, the global identification of secreted proteins. The researchers identified potential biomarkers from the conditioned medium of PC-3 prostate cancer cells. Their top candidates included Filamin-B and Keratin-19. Using Lifeline® human prostate epithelial cells as a normal control, the group examined the transcript expression of Keratin-19, Filamin-B, and Filamin-A (which they noticed was causally linked to Filamin-B) in LnCAP and DU145 prostate cancer cells. They found that there was no pattern of transcript expression of these targets when comparing either normal cells to cancer cells, or cancer cells with different androgen sensitivity. To further evaluate the relevance of these candidates to prostate cancer, the researchers treated LnCAP, DU145, and PC-3 cells with prostate cancer stimuli, including hypoxia, TNF-a, and R1881 (a synthetic androgen), and found that the transcriptional responses of each cell line for Filamin-A, Filamin-B, Keratin-19, and PSA differed. Additionally, the PSA transcript response did not correlate with that of the candidate biomarkers, suggesting that Filamin-A, Filamin-B, and Keratin-19 do not share common regulatory mechanisms with PSA.

To establish the clinical relevancy of their work, the authors first determined whether these candidate biomarkers could be secreted from prostate cancer cells. They found that in conditioned medium from the three prostate cancer cell lines, Filamin-A and Filamin-B were both readily detected. Keratin-19 was detected in conditioned medium from two of the three cancer cell lines. The group then evaluated the expression of Filamin-A, Filamin-B, and Keratin-19 in the plasma of prostate cancer patients. They found that both Filamin-A and Filamin-B were detected in plasma from patients suspected to have prostate cancer. Together, the results of this study demonstrate that Filamin-A and Filamin-B are plasma biomarkers that may be useful for detecting prostate cancer in patients.

 

Early- and late-term pregnancies can be dangerous for both the mother and child. Complex signaling cues regulate the transition from a quiescent uterine endometrium to an active endometrium, a process called parturition, or the process of giving birth. In particular, progesterone signaling plays a large part in this process. Progesterone signaling is regulated by two receptors, PGR-A and PGR-B. Active PGR-B regulates uterine quiescence, while an increase in PGR-A and high progesterone allow for initiation of estrogen receptor signaling and uterine contraction, resulting in labor induction. In a 2015 study, Pabona et al. evaluated the role of Kruppel-like factor 9 (KLF9) in the regulation of progesterone signaling and parturition. Previous studies had determined that mice lacking Klf9 had lower PGR-A and delayed parturition, prompting a new investigation into the role of KLF9 in human parturition. In the current study, the researchers found that women with late-term pregnancies expressed lower myometrial PGR-A than PGR-B, as well as lower KLF9. The researchers also found differential transcriptional expression of chemokines and cytokines in normal versus late-term pregnancy that may influence prolonged pregnancy.

To understand the mechanism by which KLF9 may influence the signaling pathways that regulate parturition, the authors used Lifeline® human uterine smooth muscle cells to knock down KLF9 expression and treated them with estrogen and progesterone. Following treatment with RU486, which blocks progesterone, a model of parturition was established. The authors found that loss of KLF9 in RU486-treated cells resulted in increased PGR-B and decreased levels of inflammatory cytokines important for initiation of parturition. Together, the results of this study suggest that KLF9 is important for induction of PGR-A and labor-inducing cytokines, and insufficient KLF9 levels may result in delayed parturition.

Lifeline® Reproductive Cell Types

Lifeline® has multiple male and female reproductive cell types for your research applications:

Are you using Lifeline® reproductive cell types in your research? If so, please let us know and your study could be featured here on our blog!