Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Javier Camacho
 -- 1980 2023-06-08 23:06:32 |
2 format correct
Jessie Wu
 + 2 word(s) 1982 2023-06-09 02:59:08 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Ramírez, A.; Ogonaga-Borja, I.; Acosta, B.; Chiliquinga, A.J.; De La Garza, J.; Gariglio, P.; Ocádiz-Delgado, R.; Bañuelos, C.; Camacho, J. Association between K+ Channels and Gynecological Cancers. Encyclopedia. Available online: https://encyclopedia.pub/entry/45366 (accessed on 27 July 2024).
Ramírez A, Ogonaga-Borja I, Acosta B, Chiliquinga AJ, De La Garza J, Gariglio P, et al. Association between K+ Channels and Gynecological Cancers. Encyclopedia. Available at: https://encyclopedia.pub/entry/45366. Accessed July 27, 2024.
Ramírez, Ana, Ingrid Ogonaga-Borja, Brenda Acosta, Andrea Jazmín Chiliquinga, Jaime De La Garza, Patricio Gariglio, Rodolfo Ocádiz-Delgado, Cecilia Bañuelos, Javier Camacho. "Association between K+ Channels and Gynecological Cancers" Encyclopedia, https://encyclopedia.pub/entry/45366 (accessed July 27, 2024).
Ramírez, A., Ogonaga-Borja, I., Acosta, B., Chiliquinga, A.J., De La Garza, J., Gariglio, P., Ocádiz-Delgado, R., Bañuelos, C., & Camacho, J. (2023, June 08). Association between K+ Channels and Gynecological Cancers. In Encyclopedia. https://encyclopedia.pub/entry/45366
Ramírez, Ana, et al. "Association between K+ Channels and Gynecological Cancers." Encyclopedia. Web. 08 June, 2023.
Association between K+ Channels and Gynecological Cancers
Edit
This entry is adapted from the peer-reviewed paper 10.3390/ph16060800

Ion channels are integral membrane proteins that allow the passage of ions through the plasma membrane and participate in diverse biological functions, from regulating the membrane potential to promoting signal transduction, contraction, and secretion, among many others. The potassium channel family is the most widely distributed group of ion channels, composed of dimers or tetrameric integral membrane proteins that regulate the flux of potassium ions. They are divided into four families based on the classification of the International Union of Basic and Clinical Pharmacology (IUPHAR): (i) voltage-gated K+ channels (Kv) encoded by forty genes in twelve subfamilies, (ii) inwardly rectifying K+ channels, (Kir) encoded by fifteen genes classified in seven subfamilies, (iii) calcium- and sodium-activated potassium channels (KCa, KNa) encoded by eight genes in five subfamilies, and (iv) two-pore domain K+ channels (K2P) encoded by fifteen genes in six subfamilies. Potassium channels are aberrantly expressed in different cancer cell lines and cancer tissues, and there is mounting evidence that supports the association of potassium channels with the hallmarks of cancer, including cell proliferation, invasion, and migration; in accordance, blocking or suppressing their expression or activity has antineoplastic features in different types of tumors in both, in vitro and in vivo studies, strongly suggesting them as candidates for targeted therapy.

gynecological cancer personalized medicine ion channels ovarian cancer endometrial cancer cervical cancer

1. Endometrial Cancer

In endometrial cancer (EC), overexpression of potassium channels has been reported in several cell lines and tumor tissues [1]. The intermediated-conductance Ca2+-activated K+ channel 3.1. (KCa3.1, KCNN4) mRNA expression and the corresponding protein level (detected by Western blot) are increased in EC tissues, compared to normal tissue and atypical hyperplasia. Inhibition of KCNN4 activity by blocking the channel with clotrimazole or TRAM-34, or knockout with siRNA, reduces HEC1-A and KLE cell proliferation by arresting the cells in the G0/G1 phase [2], and this was associated with reduced expression of cyclin D1 and cyclin E1 in HEC1-A and Ishikawa cells [3]. On the contrary, activation of KCNN4 induces cell cycle progression to G1 phase [2]. Furthermore, treatment of HEC1-A and Ishikawa cells with TRAM-34 reduces migration with a reduction in MMP-2 expression [3]. In nude mice with tumors of HEC1-A cells that are treated with TRAM-34 or clotrimazole, results showed smaller tumor development versus control groups [2]. Other potassium channel blockers, such as glibenclamide (GLI), 4-aminopyridine (4-AP), and tetraethylammonium (TEA), suppress cell proliferation, besides GLI and 4-AP also reduce migration in the HEC1-A cell line [4].
Another K+ channel, the large-conductance voltage and Ca2+-activated K+ channel (KCa1.1, KCNMA1), is involved in cancer cell proliferation and migration, and it is aberrantly expressed in many types of tumors, including cervical [5], ovarian [6], and endometrial cancers [7][8]. It is involved in cancer cell proliferation and migration. Overexpression of KCNMA1 in HEC-1-B cells by transient transfection increases viability, promotes the cell cycle to S and G2/M phases, and favors migration. Furthermore, the contrary effect is obtained with the inhibitor IBTX or knockdown of KCNMA1. These treatments reduce proliferation and migration, and in vivo studies show a diminished tumor growth rate in nude mice with HEC-1-B xenografts [8]. In 185 tissue samples of type I endometrial cancer, protein expression of KCNMA1 by immunohistochemistry was compared with 40 normal endometrium tissues and 38 atypical endometrial hyperplasia tissues; a significantly higher expression was found in all layers of type I endometrial cancer, and there was more correlation with higher FIGO (International Federation of Gynecology and Obstetrics) stages and lymph node metastasis samples, suggesting the association of these channels with poor prognosis [7]. Thus, despite the need of supplementary research to validate prognosis features and experimental research to underline the mechanism by which KCNMA1 is involved in EC, it may be a future candidate for personalized medicine schemes in patients displaying aberrant expression of the channel.
Potassium channels may have a tumor promoting role in EC, as it occurs in other malignancies. Thus, the fine regulation of these channels by EC-associated factors, including hormones, also deserves further investigation.

2. Ovarian Cancer

Potassium channels have been associated with ovarian cancer (OC) progression and prognosis. One of the most studied K+ channels in cancer, the ether-à-go-go-related potassium channel 1 (KV11.1, KCNH2), is widely overexpressed in many types of cancer and promotes proliferation, migration, and invasion [9]. In ovarian cancer (OC) tumor tissues, higher KCNH2 mRNA and protein expression were found when compared with adjacent non-tumor tissues, and the higher expression of KCNH2 has been associated with lymph node metastasis (LNM) and distant metastasis [10]. One study of the DNA methylation profile of clear cell OC tumors found hypermethylation and reduced mRNA expression of KCNH2; the low levels of KCNH2 in clear cell OC was associated with good prognosis, emphasizing the tumor-promoting role of these channels [11]. To the contrary, microarray analysis of the potassium calcium-activated channel subfamily N member 3 (KCa2.3, KCNN3) revealed a significantly lower expression in OC tissues and in drug-resistant OC, compared with normal tissue and sensitive tissues, respectively. Furthermore, lower staining of KCNN3 by immunohistochemistry was observed in 33 of 57 tissues of OC, compared to a higher expression observed in 6 controls, and a 75% lower expression in drug-resistant tissues compared to 37% in drug-sensitive tissues was observed. These latter findings were correlated with shorter disease-free survival in samples with lower KCNN3 expression, suggesting that KCNN3 could be a tumor suppressor, therapeutic target, and a marker of poor prognosis in OC [12].
The pattern expression of potassium channels in OC may reveal the potential role of these channels as tumor promoters or suppressors. The specific therapeutic approach inhibiting or inducing the expression of certain potassium channels may give advantages for each patient in personalized medicine.

3. Cervical Cancer

Several potassium ion channels have been implicated in the progression of cervical cancer (CCa). For example, KV10.1 (KCNH1) is associated with proliferation, malignant transformation, and tumor growth, and various studies have been conducted to study inhibitors of KCNH1, such as tetrandrine (30 mg/kg/day), that reduce CCa tumor growth in vivo [13]. Likewise, blockage of the KV3.4 (KCNC4) channel with BDS-II inhibits the migration of HeLa cells by 46%, reduces the expression of vimentin, inactivates the AKT pathway by diminishing phospho-AKT (Ser473), and increases activation of PTEN, which is a negative regulator of the AKT pathway and a tumor suppressor [14]. Detecting early stages of cancer development is one of the key factors for a successful treatment. In the case of KCNMA1 (KCa1.1), it has been proposed as an early marker for CCa since higher immunostaining of the protein is more prominent in high-grade dysplasia and cervical cancer tissues [5]. Western blot analysis was used to determine the voltage-gated potassium channel KV1.1 (KCNA1) protein expression, showing its overexpression in CCa cell lines (HeLa, SiHa, and C-33A) compared to normal epithelia tissue, and its knockdown reduces the migration, proliferation, and invasion of HeLa cells associated with decreased Hhg and Wnt protein levels and mitochondrial capacity. Besides, in 20 CCa tissue samples from patients, increased expression of KV1.1 was correlated with poor prognosis and reduced survival time, which suggest KV1.1 as a potential biomarker for tumor development and survival rate in cervical cancer [15]. To improve chemotherapy outcomes, a widely used alternative is to sensitize cancer cells to cytotoxic drugs by increasing their permeability, considering that several anticancer drugs, such as cisplatin and doxorubicin, have low membrane permeability. Bukhari et al. found that the activation of the intermediate conductance Ca2+-activated K+ channels (KCa3.1), which is upregulated in CCa cells, induces H33258 uptake, a cytotoxic DNA-binding cationic dye [16].
The use of specific and general inhibitors of potassium channels is a very promising approach to improve CCa therapy. While some inhibitors may be used as to decrease the malignant properties of cancer cells, the overexpression of some ion channels may also be used to facilitate the entry of anticancer drugs. In this type of cancer, the precise regulation of these channels by human papilloma virus (HPV) oncogenes and hormones is also warranted.
The differential expression of potassium channels in gynecological cancers strongly suggests that different molecular mechanisms are involved in favoring tumor development. Some potassium channels are overexpressed, while others are downregulated, strongly suggesting that potassium currents or membrane potential are not the sole mechanism involved. The potential association of potassium channels with other proteins deserves further investigation.
Table 1. Preclinical and clinical evidence associating potassium channels with gynecological cancers.
Channel In Vitro Animal Models Clinical Observations Reference
Endometrial Cancer
KV11.1 High expression of KCNE and HERG genes in the AN3-CA, KLE, and Ishikawa cell lines.   Higher frequency of RNA and protein expression in primary human tumors compared to non-cancerous tissues. [17][18]
KCa1.1 Silencing with siRNA reduced cell proliferation, cell migration, and p-MEK1/2 and p-ERK1/2 expression in Ishikawa cells.
Overexpression promotes cell proliferation and migration, and blockage with IBTX reduces cell proliferation in HEC-1-B cells.		 Silencing in xenografts transplanted in nude mice produced smaller tumors compared to control mice. Higher protein staining in type I endometrial adenocarcinoma tissue compared to normal and atypical endometrial tissues. [7][8]
KCa3.1 Downregulation by siRNA in HEC-1-A and KLE cells inhibits proliferation.
Silencing by shRNA or blockage with TRAM-34 reduces cell cycle progression, and TRAM-34 diminishes migration and MMP2 expression in HEC-1-A and Ishikawa cells.		 TRAM-34 and clotrimazole reduced tumor formation of HEC-1-A cells in nude mice. Higher expression of mRNA and protein levels in endometrial cancer tissues compared to normal tissues. [2][3]
Cervical cancer
KV1.1 Knockdown suppresses cell proliferation, migration, invasion, and protein levels of Hhg and Wnt1 in HeLa cells. Knockdown in HeLa cells generated smaller xenograft tumors and prolonged survival in nude mice. Higher protein expression in CCa tissues correlates with poor prognosis. [15]
KV3.4 Inactivation of the AKT pathway and inhibition of cell migration by blockage with BDS-II in Hela cells.     [14]
KV10.1 Higher expression in HeLa, SiHa, and primary cultures of cervical cancer.
Imipramine and astemizole decrease channel expression and increase apoptosis in E6/E7-transfected keratinocytes.
Decreased proliferation and increased apoptosis of HeLa, SiHa, CaSki, INBL, and C-33A cells with astemizole treatment.
Decreased mRNA and proliferation with calcitriol treatment in the SiHa cell line.		 Inhibition of tumor growth in xenograft mice with tetrandrine treatment.
Increased mRNA and protein expression in CCa tissues of transgenic mice K14E7 treated with estrogens.		 Higher expression in high-grade cervical lesions compared to low-grade lesions and normal tissues. [19][20][21][22][23]
Kir6.2 Overexpression of mRNA in HeLa cells, and blockage with glibenclamide reduces cell viability.   Higher expression in invasive tumors compared to low or non-invasive tumors. [24]
KCa1.1   Estradiol treatment increased protein and mRNA expression in K14E7 transgenic mice with CCa. Higher intensity of immunostaining in biopsies of carcinoma in situ. [5]
KCa3.1 Downregulation by siRNA increased apoptosis in HeLa cells.
Increased uptake of dye H33258 dependent on KCa3.1 is observed in cervical carcinoma cell lines (CXT) compared to nonmalignant cervical epithelial cell strains (HCX).
Clotrimazole reduces mRNA expression and changes HeLa cell morphology.		   mRNA and protein overexpression in cervical cancer tissues. [16][25][26]
Ovarian cancer
K2p2.1
K2p10.1		 Curcumin increases late apoptosis and decrease proliferation in SK-OV-3 and OVCAR-3 cells.   Expression is increased in cancer samples compared to normal ovarian samples. [27]
K2p9.1 Reduction in proliferation and increase in late apoptosis in SK-OV-3 and OVCAR-3 cells with methanandamide treatment.   Significant correlation of immunostaining with tumor stage in patient biopsies. [28]
KV10.1 KV11.1 4-aminopyridine and tetraethylammonium inhibited proliferation in SK-OV-3 cells.
Imipramine increases apoptosis levels and decreases proliferation in SK-OV-3 cells.
Ergtoxin inhibits the proliferation of SK-OV-3 cells.		   Higher expression in OC tissues compared to noncancerous tissue. [29][30]
KV10.1 siRNA targeting sensitizes SK-OV-3 and TYK cells to cisplatin-induced apoptosis.   High expression compared to normal tissues. [31]
KV11.1 Berberine reduces mRNA and protein levels in SK-OV-3 cells. Berberine decreases tumor growth in xenografts compared to the control group. High protein expression in tumor tissues compared to non-tumor tissues. [10]
KCa1.1 Correlation of miR-31 levels and resistance to cisplatin in A2780 cells.   Loss of expression is associated with cisplatin resistance. [32]
KCa2.3     Low mRNA and protein expression in samples of ovarian serous cystadenocarcinomas compared to normal ovarian tissues and correlated with shorter disease-free and overal survival. [12]

References

  1. Costa, B.P.; Nunes, F.B.; Noal, F.C.; Branchini, G. Ion Channels in Endometrial Cancer. Cancers 2022, 14, 4733.
  2. Wang, Z.H.; Shen, B.; Yao, H.L.; Jia, Y.C.; Ren, J.; Feng, Y.J.; Wang, Y.Z. Blockage of intermediate-conductance-Ca(2+) -activated K(+) channels inhibits progression of human endometrial cancer. Oncogene 2007, 26, 5107–5114.
  3. Zhang, Y.; Feng, Y.; Chen, L.; Zhu, J. Effects of Intermediate-Conductance Ca(2+)-Activated K(+) Channels on Human Endometrial Carcinoma Cells. Cell Biochem. Biophys. 2015, 72, 515–525.
  4. Erdem Kis, E.; Tiftik, R.N.; Al Hennawi, K.; Un, I. The role of potassium channels in the proliferation and migration of endometrial adenocarcinoma HEC1-A cells. Mol. Biol. Rep. 2022, 49, 7447–7454.
  5. Ramírez, A.; Vera, E.; Gamboa-Domínguez, A.; Lambert, P.; Gariglio, P.; Camacho, J. Calcium-activated potassium channels as potential early markers of human cervical cancer. Oncol. Lett. 2018, 15, 7249–7254.
  6. Oeggerli, M.; Tian, Y.; Ruiz, C.; Wijker, B.; Sauter, G.; Obermann, E.; Güth, U.; Zlobec, I.; Sausbier, M.; Kunzelmann, K.; et al. Role of KCNMA1 in breast cancer. PLoS ONE 2012, 7, e41664.
  7. Wang, F.; Chen, Q.; Huang, G.; Guo, X.; Li, N.; Li, Y.; Li, B. BKCa participates in E2 inducing endometrial adenocarcinoma by activating MEK/ERK pathway. BMC Cancer 2018, 18, 1128.
  8. Li, N.; Liu, L.; Li, G.; Xia, M.; Du, C.; Zheng, Z. The role of BKCa in endometrial cancer HEC-1-B cell proliferation and migration. Gene 2018, 655, 42–47.
  9. He, S.; Moutaoufik, M.T.; Islam, S.; Persad, A.; Wu, A.; Aly, K.A.; Fonge, H.; Babu, M.; Cayabyab, F.S. HERG channel and cancer: A mechanistic review of carcinogenic processes and therapeutic potential. Biochim. Biophys. Acta Rev. Cancer 2020, 1873, 188355.
  10. Zhi, D.; Zhou, K.; Yu, D.; Fan, X.; Zhang, J.; Li, X.; Dong, M. hERG1 is involved in the pathophysiological process and inhibited by berberine in SKOV3 cells. Oncol. Lett. 2019, 17, 5653–5661.
  11. Cicek, M.S.; Koestler, D.C.; Fridley, B.L.; Kalli, K.R.; Armasu, S.M.; Larson, M.C.; Wang, C.; Winham, S.J.; Vierkant, R.A.; Rider, D.N.; et al. Epigenome-wide ovarian cancer analysis identifies a methylation profile differentiating clear-cell histology with epigenetic silencing of the HERG K+ channel. Hum. Mol. Genet. 2013, 22, 3038–3047.
  12. Liu, X.; Wei, L.; Zhao, B.; Cai, X.; Dong, C.; Yin, F. Low expression of KCNN3 may affect drug resistance in ovarian cancer. Mol. Med. Rep. 2018, 18, 1377–1386.
  13. Wang, X.; Chen, Y.; Li, J.; Guo, S.; Lin, X.; Zhang, H.; Zhan, Y.; An, H. Tetrandrine, a novel inhibitor of ether-à-go-go-1 (Eag1), targeted to cervical cancer development. J. Cell Physiol. 2019, 234, 7161–7173.
  14. Sim, H.J.; Song, M.S.; Lee, S.Y. Kv3 channels contribute to cancer cell migration via vimentin regulation. Biochem. Biophys. Res. Commun. 2021, 551, 140–147.
  15. Liu, L.; Chen, Y.; Zhang, Q.; Li, C. Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage. Channels 2019, 13, 321–330.
  16. Bukhari, M.; Deng, H.; Sipes, D.; Ruane-Foster, M.; Purdy, K.; Woodworth, C.D.; Sur, S.; Samways, D.S.K. KCa3.1-dependent uptake of the cytotoxic DNA-binding dye Hoechst 33258 into cancerous but not healthy cervical cells. J. Biol. Chem. 2021, 296, 100084.
  17. Cherubini, A.; Taddei, G.L.; Crociani, O.; Paglierani, M.; Buccoliero, A.M.; Fontana, L.; Noci, I.; Borri, P.; Borrani, E.; Giachi, M.; et al. HERG potassium channels are more frequently expressed in human endometrial cancer as compared to non-cancerous endometrium. Br. J. Cancer 2000, 83, 1722–1729.
  18. Suzuki, T.; Takimoto, K. Selective expression of HERG and Kv2 channels influences proliferation of uterine cancer cells. Int. J. Oncol. 2004, 25, 153–159.
  19. Díaz, L.; Ceja-Ochoa, I.; Restrepo-Angulo, I.; Larrea, F.; Avila-Chávez, E.; García-Becerra, R.; Borja-Cacho, E.; Barrera, D.; Ahumada, E.; Gariglio, P.; et al. Estrogens and human papilloma virus oncogenes regulate human ether-à-go-go-1 potassium channel expression. Cancer Res. 2009, 69, 3300–3307.
  20. Ortiz, C.S.; Montante-Montes, D.; Saqui-Salces, M.; Hinojosa, L.M.; Gamboa-Dominguez, A.; Hernández-Gallegos, E.; Martínez-Benítez, B.; Del Rosario Solís-Pancoatl, M.; Garcia-Villa, E.; Ramírez, A.; et al. Eag1 potassium channels as markers of cervical dysplasia. Oncol. Rep. 2011, 26, 1377–1383.
  21. de Guadalupe Chávez-López, M.; Hernández-Gallegos, E.; Vázquez-Sánchez, A.Y.; Gariglio, P.; Camacho, J. Antiproliferative and proapoptotic effects of astemizole on cervical cancer cells. Int. J. Gynecol. Cancer 2014, 24, 824–828.
  22. Avila, E.; García-Becerra, R.; Rodríguez-Rasgado, J.A.; Díaz, L.; Ordaz-Rosado, D.; Zügel, U.; Steinmeyer, A.; Barrera, D.; Halhali, A.; Larrea, F.; et al. Calcitriol down-regulates human ether a go-go 1 potassium channel expression in cervical cancer cells. Anticancer Res. 2010, 30, 2667–2672.
  23. Farias, L.M.; Ocaña, D.B.; Díaz, L.; Larrea, F.; Avila-Chávez, E.; Cadena, A.; Hinojosa, L.M.; Lara, G.; Villanueva, L.A.; Vargas, C.; et al. Ether a go-go potassium channels as human cervical cancer markers. Cancer Res. 2004, 64, 6996–7001.
  24. Vazquez-Sanchez, A.Y.; Hinojosa, L.M.; Parraguirre-Martinez, S.; Gonzalez, A.; Morales, F.; Montalvo, G.; Vera, E.; Hernandez-Gallegos, E.; Camacho, J. Expression of K(ATP) channels in human cervical cancer: Potential tools for diagnosis and therapy. Oncol. Lett. 2018, 15, 6302–6308.
  25. Liu, L.; Zhan, P.; Nie, D.; Fan, L.; Lin, H.; Gao, L.; Mao, X. Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical Cancer. Med. Sci. Monit. Basic Res. 2017, 23, 45–57.
  26. Zhan, P.; Liu, L.; Nie, D.; Liu, Y.; Mao, X. Effect of inhibition of intermediate-conductance-Ca(2+)-activated K(+) channels on HeLa cell proliferation. J. Cancer Res. Ther. 2018, 14, S41–S45.
  27. Innamaa, A.; Jackson, L.; Asher, V.; van Schalkwyk, G.; Warren, A.; Keightley, A.; Hay, D.; Bali, A.; Sowter, H.; Khan, R. Expression and effects of modulation of the K2P potassium channels TREK-1 (KCNK2) and TREK-2 (KCNK10) in the normal human ovary and epithelial ovarian cancer. Clin. Transl. Oncol. 2013, 15, 910–918.
  28. Innamaa, A.; Jackson, L.; Asher, V.; Van Shalkwyk, G.; Warren, A.; Hay, D.; Bali, A.; Sowter, H.; Khan, R. Expression and prognostic significance of the oncogenic K2P potassium channel KCNK9 (TASK-3) in ovarian carcinoma. Anticancer Res. 2013, 33, 1401–1408.
  29. Asher, V.; Khan, R.; Warren, A.; Shaw, R.; Schalkwyk, G.V.; Bali, A.; Sowter, H.M. The Eag potassium channel as a new prognostic marker in ovarian cancer. Diagn. Pathol. 2010, 5, 78.
  30. Asher, V.; Warren, A.; Shaw, R.; Sowter, H.; Bali, A.; Khan, R. The role of Eag and HERG channels in cell proliferation and apoptotic cell death in SK-OV-3 ovarian cancer cell line. Cancer Cell Int. 2011, 11, 6.
  31. Hui, C.; Lan, Z.; Yue-li, L.; Li-lin, H.; Li-lin, H. Knockdown of Eag1 Expression by RNA Interference Increases Chemosensitivity to Cisplatin in Ovarian Cancer Cells. Reprod. Sci. 2015, 22, 1618–1626.
  32. Samuel, P.; Pink, R.C.; Caley, D.P.; Currie, J.M.; Brooks, S.A.; Carter, D.R. Over-expression of miR-31 or loss of KCNMA1 leads to increased cisplatin resistance in ovarian cancer cells. Tumour Biol. 2016, 37, 2565–2573.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Oncology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Ana Ramírez
,
Ingrid Ogonaga-Borja
,
Brenda Acosta
,
Andrea Jazmín Chiliquinga
,
Jaime de la Garza
,
Patricio Gariglio
,
Rodolfo Ocádiz-Delgado
,
Cecilia Bañuelos
,
Javier Camacho
View Times: 270
Revisions: 2 times (View History)
Update Date: 09 Jun 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback